Do Firstbeat offer more in 2009 than Forbes and Ursula Carlile in 1959?

In recent postings I have been exploring the possibility that measurements of Heart rate Variability (HRV) might provide a useful way of detecting over-training and of adjusting training load to achieve optimum outcome. In response to a query from Ewen, on 30^th June I had looked at the question of which commercially available heart rate monitor might provide the most useful measurement of HRV.  I had attempted to compare the merits of the products offered by Polar and by Suunto.  In fact, this was a frustrating task because the material presented on the websites of the two companies does not provide enough details of the principles underlying their procedures for using HRV to monitor training load and over-training, nor adequate evidence that using their devices leads to improved outcomes of training.

However I had concluded that the most promising current approach uses software developed by the Finnish company Firstbeat Technologies.  Firstbeat software can read the data from either the Suunto t6 or the Polar RS800. Suunto have incorporated Firstbeat software into their own Training Manager software and have committed themselves more heavily to the utilization of Firstbeat software.  Some  of the measurments such as Training Effect (see below) can be read directly from Suunto HRMs  such as the t3,  t4 and t6r, during the training session.  Nonetheless, the primary input required for Firstbeat software is a record of inter-beat interval in a series of heart beats recorded under whatever circumstances one is interested in, whether than be during rest or exercise, and this data can be provided by either the Suunto t6 or Polar RS800, though the full analysis cannot be performed until after the training session is over. 

Therefore in deciding between Suunto and Polar for the purpose of measuring HRV, the major issues is likely to be reliability of the recorded data, the size of the data store and the ease with which it can be read by Firstbeat software.  I have not looked into any of these questions, though issues such as susceptibility to interference arising from power lines or nearby HRM’s worn by other athletes are addressed in a comparison of Suunto and Polar devices by PC Coach

(http://www.pccoach.com/newsletters/Nov05/speedist5.htm ) 

Note added 5 July 2009:   If you are interested in comparing other practical aspects of the Polar PS800CX and the Suunto t6r, such as convenience for use during a triathlon, or the utility of the software provided by Suunto and Polar for planning of your training sessions, Jan Musil provides an excellent comparison at:

http://runtotri.blogspot.com/2009/01/polar-rs800cx-or-suunto-t6c-that-is.html

As far as I can see, despite differences in detail, both companies provide technically sound equipment.    However my present interest is in the Firstbeat software. 

KIHU and Firstbeat

Firstbeat is a spin-off company created by members of KIHU – Research Institute for Olympic Sports, located in Jyväskylä, Finland.  KIHU researchers have conducted a number of very informative studies of HRV over the past decade.  The senior investigator in many of these investigations is Heikki Rusko, a well known exercise physiologist.  By examination of both the scientific publications produced by KIHU and by reading the material presented on the Firstbeat technologies website, it is possible to get a reasonable understanding of what the Firstbeat software has to offer, though not quite as clear a picture as I would like to have.

 

In my opinion the peer reviewed publications from KIHU provide only moderate, but nonetheless tantalizing, support for the proposal that HRV and related measures would provide a reliable estimate of training stress.  The material presented on the website provides more information about what computations the Firstbeat software performs, but many details are missing, and the quality of some of the crucial scientific evidence falls below that I would expect in a peer reviewed scientific publication.  Nonetheless, some of the material on the Firstbeat website (especially the downloadable white papers) appears to have been written by exercise physiologists rather than marketing personnel.  Maybe this makes it harder to read but ultimately, more worthwhile. So in this posting I will present a personal overview of what I regard as the most relevant outputs from the Firstbeat software

The three outputs most relevant to the scientific assessment of athletic training are:

EPOC: an estimate of oxygen debt acquired during a training session.  This provides a measure of the stress on the cardio-respiratory system resulting from the session;

Training Effect: an estimate of the potential benefit (or in some instances, degree of  overreaching)  from a training session;

Recovery index:  a measure of autonomic nervous system balance that is potentially a useful indicator of over-training.

It should be noted that Firstbeat produce three main software packages, each of which is specialized for different users:

Firstbeat ATHLETE (FBA), which calculates EPOC, Training effect and provides guidance on planning a training program.  However FBA does not provide an analysis of recovery.  While it does provide guidance that should minimize the risk of over or under-training, the planning is based on the estimated Training Effect of recent sessions rather than on a direct measurement of the degree of recovery immediately prior to the next session.   

Firstbeat SPORTS, which calculates EPOC, training effect and also provides a detailed analysis of stress and recovery.  This includes a recovery analysis based on overnight recording, and charts of stress and recovery throughout the day.  This analysis takes account of cumulative stress not only of recent training sessions, but also of other life events. This software is designed for sports professionals

Firstbeat HEALTH, which provides detailed stress and recovery analysis. It is designed for use in studies of occupational health and therefore is not oriented towards the management of an athlete’s training program.

EPOC 

It is well known that exercise creates an oxygen debt such that oxygen uptake over a period of minutes or hours after cessation of the exercise is increased compared with baseline.  This is known as Excess Post Exercise Oxygen consumption (EPOC).  This can be measured directly in a laboratory using equipment to measure respiration.  KIHU researchers report that the oxygen debt can be predicted reliably from heart rate and respiration rate (calculated from HRV) measured during the exercise.   The EPOC measurement produced by the Firstbeat software is the predicted EPOC based on heart rate recording during exercise.  As oxygen debt only accumulates when exercise is of at least moderate intensity, EPOC generally increases with time during moderate or heavy exercise but tends to decrease with time during periods of light exercise following heavier exercise.

How good is the evidence that EPOC is a good estimate of the total accumulated stress applied to the cardiovascular system?  Firstbeat show that EPOC is strongly correlated with lactate accumulation, which is quite plausible.  However, at low workloads, such as the levels proposed by Philip Maffetone during the base-building phase, lactate accumulation is minimal, and therefore one might expect that EPOC will be small, yet some training effect on the heart would be anticipated. 

The data provided by Firstbeat in their white paper on EPOC demonstrate that at a workload corresponding to 40% of VO2max, EPOC scarcely rises at all after the first 30 minutes.  Does this indicate that long slow runs do not produce stress (and hence useful training effects) on the cardio-respiratory system?   As far as I can see this issue remains unresolved,  and I would like to see more evidence.

Furthermore the calculation of predicted EPOC requires a prior estimate of HRmax and if this is inaccurate, the calculation of EPOC will be inaccurate.

Training Effect

This is an estimate of the training benefit derived from a given training session and is computed from the peak EPOC achieved during the session  taking account of the athlete’s current activity level.  Activity level is scored on a 10 point scale largely based on current weekly training load.  The underlying principle is that an athlete with a high current activity level will require a higher value of EPOC to achieve a comparable training benefit compared with a less active athlete.   This is perfectly reasonable, but on account of the crudeness of the estimate of current fitness provided by the activity level scale, I suspect that the Training Effect value is imprecise.  Training Effect itself is quantified on a scale from 1 to 5 where 1 indicates a minor training effect and 5 or more indicates over-reaching. 

A good coach (or even a thoughtful athlete) might perhaps be able to estimate the value of a training session just as well on the basis of experience, but many of us are not wise judges of how hard we are training, and we do not all have access to a wise and experienced coach.  In principle, keeping a log of Training Effect values for the week’s sessions would probably be a more sensible guide to how effectively we are training that keeping a log of total miles or Km run  each week, yet many of us are inclined to draw psychological support from our weekly mileage total. 

However, just as a log of weekly mileage has its limitations as a measure of training, so does a log of Training Effect.  Not only is it likely to be an imprecise estimate of effects on the heart,  but in addition, Training Effect does not take adequate account of other organs of the body, especially the musculo-skeletal system.  It is highly likely that long slow distance training strengthens bones, tendons and ligaments (and conversely that running excessively long distances creates risk of musculo-skeletal injury) yet the computation of Training Effect appears to under-estimate either the benefits or risks of long slow distance running.  Furthermore, the calculation of Training Effect does not take account of the benefits derived from strength or flexibility exercises.   So it might be a little more useful that a log of weekly mileage, but it does not reflect all of the important benefits (and risks) from a  training program, and it would be foolish to plan a program guided only by measurments of Training Effect.

Recovery Analysis

The potentially most useful analysis provided by the Firstbeat software is the recovery analysis based on an overnight estimate of stress and recovery.  The measurement is based on recorded heart beat during a four hour period of sleep.  A quantity known as the recovery index is computed from heart rate, heart rate variability (HRV) and estimated breathing rate derived from HRV. 

Firstbeat do not say exactly how this computation is performed, but a white paper presented on the website states that the procedure  was derived by fitting a mathematical model to a large amount of data collected in many studies.  In this context, the mathematical model is an equation that estimates the balance between sympathetic and parasympathetic nervous activity using physiological information such as HRV.   The principle of deriving an equation that predicts a physiological variable of interest from the values of related physiological variables is well established in exercise physiology.  For example Daniels’ famous equation for predicting VO2 from speed and duration of a run is a quadratic equation that was derived by determining the coefficients of the quadratic equation that gave the best fit to the observed data in a large number of individuals.  It is likely that Firstbeat have used a different type of equation, based on more complex mathematics, for the prediction, but the principle of fitting observed data to a mathematical model is likely to be similar. 

Potentially the biggest limitation of this type of approach is that even if the prediction works well for the average value in a group, it might not be accurate for the individual.  This issue is most clearly illustrated by the linear equations that have been proposed to predict HRmax from age. In some instances, the prediction is quite inaccurate.   The relationship between HRmax and age is a notorious example of an unreliable mathematical model of physiological data.  Nonetheless, I would like to see more data demonstrating the reliability of the model used by Firstbeat to estimate the recovery index.

Firstbeat quite rightly point out that the absolute value of the  recovery index is not very meaningful.  What is required is a measure of change from baseline within the individual.  However they do not present clear evidence for the consistency of changes from baseline within individuals who develop over-training syndrome.   The most relevant supportive data comes for a study by Hynynen and colleagues comparing over-trained with non over-trained  athletes (  Hynynen, E., Uusitalo, A., Konttinen, N. & Rusko H. (2006). Heart rate variability during night sleep and after awakening in overtrained athletes. Medicine and Science in Sports and Exercise 38(2): 313-317).

However the data relevant to the recovery index was not included in the published peer reviewed paper reporting the study but is only available in a white paper on the Firstbeat website.   Ironically, the published article actually concluded that overnight HRV did not distinguish between the over-trained and non-over-trained athletes, whereas measurement of change in HRV on rising did.   In contrast, the table of data presented in the Recovery white paper on the Firstbeat website does indicate that the stress/recovery index computed from overnight values by the Firstbeat software distinguished between the well recovered and poorly recovered state in 7 athletes.  Unfortunately, the white paper provides no indication of how this data was selected. 

I am intrigued by the possible utility of the recovery index and would be very interested to try this out myself.  However for the time being I will persist with my own amateur system described in my post on 26th June.  My system provides me with the ability to study the shape of the ECG  T wave as well as HRV.  In my analysis, the most informative estimate  of balance between sympathetic and parasymatheic activity is provided by the Poincare analysis of HRV.  This analysis assesses the ratio of high frequency variation (presumed closely associated with recuperative parasympathetic activity) to low frequency variation (predominantly determined by sympathetic activity)  by comparing the length of the two axes of the ellipse which I presented in my posting on 26th June.  Unfortunately, the interpretation of the Poincare analysis is not quite as simple as described in my posting on 26th June.  It is possible that the computations done by Firstbeat software are more reliable.  On the other hand, the evidence presented by Firstbeat is scarcely any more convincing than the data on ECG T waves presented by Forbes and Ursula Carlile to the Australian  Sports Medicine Association  in 1959.  As I described in my post on 30^th June, the report by Forbes and Ursula Carlile demonstrated that in selected cases, flattening of the T waves corresponds very closely to deterioration in performance due to over-training.  The presentation of data on individual subjects or small groups of subjects can look very impressive, but what I would like to see is evidence showing how well the Firstbeat procedure works for an unselected sample of athletes.

Conclusion

The available evidence does suggest that HRV measurements can provide a useful assessment the quality of training and might detect over-training.  I think that for any athlete who can afford the cost, and is prepared to interpret the data thoughtfully, a Suunto t6 with Firstbeat software (or maybe a Polar RS800 with Firstbeat software) would be a worthwhile investment.  However I am disappointed that half a century after the thought provoking presentation by Forbes and Ursula Carlile to the Australian Sports Medicine Association in 1959, it is still difficult to find publicly accessible data that would allow an objective evaluation of the reliability of measurements of autonomic nervous system function for the purpose of detecting over-training.

Should you buy a HRM that measures HRV?

In response to my recent post on over-training and Heart Rate Variability (HRV),  Ewen asked if I had an opinion about which Heart Rate Monitor with capacity to measure HRV might be best.  I have not yet purchased such a device.  Before I offer my tentative thoughts on what might be the best device to buy, it is worth a brief deviation back to the Australia of my childhood in the 1950’s.

A trip back to Australia in the 1950’s

In those days, Australia dominated the world in several sports, but especially in swimming.  The really memorable character was Dawn Fraser, who won gold in the 100m freestyle in Melbourne (1956), Rome (1960) and Tokyo (1964).  Among the men, two of the greats were John Konrads and Murray Rose. A feature of the Rome Olympics was the battle between Konrads and Rose, with Rose winning gold in the 400m freestyle and Konrads in the 1500m.  Konrads held the world 400m record at the time.   During his career he broke multiple world records over distances from 220 yards to 1650 yards.  

What has this got to do with measuring over-training?  Following my recent posting on Heart Rate Variability, Mystery Coach sent me a very interesting report which Forbes Carlile and his wife Ursula presented to the Australian Sports Medicine Association in April 1959, entitled ‘T wave changes in strenuous exercise’.  Forbes Carlile was in those days a giant figure in swimming coaching, in Australia and internationally.  Carlile and his wife had recorded over 500 ECGs from swimmers, cyclists and oarsmen, in many cases performing recordings at different points in the season and relating these recordings to changes in performance

The main conclusion of the report was that stressful training or racing produces a decrease in amplitude or sometimes complete inversion of  T waves in the ECG.  Carlile and his wife reported:  ‘In general the sportsmen with a relatively light training load gave a series of practically unchanged electrocardiograms whereas those who were training strenuously frequently showed T wave changes in all leads.’

The pictures of the ECG traces were dramatic.  For me, one of the fascinating contrasts was between the recordings for John Konrads and those for several other top level swimmers.  The three recordings for Konrads were done at the beginning of hard training at the end of November 1958, and then again immediately before and after a 440 yd race on 28^th January 1959.  Unlike the pattern seen in the other top level athletes, Konrads’  T wave amplitude increased during hard training, and remained unaffected by the race. However for several other top-level swimmers, their T waves showed quite perceptible flattening during periods of intense training.  In these instances, the decrease in T wave amplitude was associated with deterioration in performance.

Carlile and his wife concluded: ‘we suggest that serial electrocardiograms offer a practical and scientific means of guiding the sportsman in his training.’  Examination of the ECG traces provided in their report made it very difficult to disagree.  Though in light of the fact that Dawn Fraser bestrode Australian swimming like a colossal cheeky Amazon at the time, one wonders about the use of the word ‘sportsman’ – but the 1950’s were of course over before another famous but slightly cheeky Australian woman, Germaine Greer, turned not just our T waves, but our attitudes upside down with ‘The Female Eunuch’.

What has happened to T waves since 1959?

In fact we now know quite a lot more about the things that produce a change in T waves.  T waves are the most labile feature of the ECG and can be affected by many stresses on the body.  One unifying feature is that T wave amplitude is diminished when the sympathetic nervous system is overactive.  By performing scans of the heart after administering a radioactive tracer substance called I¹²³-MIBG , which competes with noradrenaline to bind to the receptors on the surface of cells in the heart that mediate the effects of the sympathetic nervous system, it is possible to show that over-activity of the sympathetic nervous system is associated with suppression of the T waves. 

Thus, in principle, T wave suppression appears to be a good candidate to assess the form of over-training characterized by excess sympathetic activity.   There is of course a problem that anxiety also causes over-activity of the sympathetic nervous system, and can cause suppression of T waves.  Therefore assessment of T waves would only be useful if interpreted in light of other features affecting the physical and mental state of the athlete. 

I do not know whether athletes at the Australian Institute of Sport still have serial ECG’s to assess training stress but I suspect this is unlikely.   Since the 1990’s the emphasis has shifted from the shape of the ECG waveform to heart rate variability, but the fact that non-invasive assessment of the  effects of the autonomic nervous system on the heart has been possible for half a century, yet there is no widespread accepted procedure, makes me cautious in offering any advice.

Back to the measurement of HRV

Despite promising findings regarding the use of HRV to adjust training schedules (as reported by Kiviniemi and colleagues in the study I described on my blog posting yesterday), the situation is complex, so I think that investment in a HRM capable of recording HRV is a speculative investment.  They are not cheap, though if you can afford it and regard it as an interesting tool for investigation rather than a certain answer to the question of how to adjust training load, then I think it might be worthwhile. 

The two companies that have invested extensively in HRV technology are Suunto and Polar.  As a person with a wish to understand the underlying physiology, I find the websites of both companies very frustrating.  Both companies have clearly recognized that there is no simple measurement that applies to all individuals under all circumstances and both have developed ways of calculating training stress that takes account of the characteristics and situation of the individual.

Polar RS800

As mentioned in my blog recently, for assessment of over-training, Polar appear to place the main emphasis on 5 measurements performed on standing up from relaxed resting. This is a variant of the traditional orthostatic test, and involves assessment of changes in heart rate and heart rate variability.  In my post yesterday I gave a link to the Polar website.  It might also be useful to read the second part of this document prepared by the Heart Rate Monitor Shop in which they describe the OwnOptimizer test performed using Polar RS800.

http://www.heartratemonitor.co.uk/Manuals/RS800/ch09.html#N119D3

My main concern about Polar’s OwnOptimizer is that it does not employ data based on the body’s response to a training session, and I am not sure how easy it is to derive estimates of autonomic function during training or during other activities of daily living from the Polar RS800.

Note added 30 June 09 (22:00): I have discovered that FirstBeat Technolgies software can read the data from a Polar RS800.  Therefore, it appears that the various useful computations that I attribute to the Sunto T6 when used in conjuntion with the First Beat Technologies software  might also be achieved using the Polar RS800.  I am frustrated by the fact that neither the Polar website or Suunto website make it clear that the capability of their devices might be mproved by use of Firstbeat Technologies software.

 

Suunto t6

The Suunto t6, when used  in conjunction with software developed by Firstbeat Technologies appears to provide useful information about autonomic function at any time of the day or night.  As far as I can see the recommended way to detect over-training is from overnight recordings.  The software measures what are described as ‘stress reactions’ during sleep, and if these continue throughout the night, the athlete is at risk of over-training.  The software also produces two potentially informative quantities related to stress during training: training effect (an estimate of the stress on the body arising from training session) and EPOC (an estimate of the body’s additional oxygen requirement post exercise, estimated from HRV measurements). 

Useful information about the Suunto t6 is provide by Eddie Fletcher, a indoor rowing coach with international credentials and a clientele that includes international indoor rowing champions.

 http://www.fletchersportscience.co.uk/ 

He has written some interesting articles for Peak Performance. The following article from PP 237 is available on his website:

http://www.fletchersportscience.co.uk/uploads/img4668277a5a6191.pdf

Emma Snowsill (Triathlon gold medal winner in Beijing) uses Suunto t6c red arrow.

 

A tentative recommendation

If I had to choose between Polar and Suunto, I would choose Suunto t6 (with the FirstBeat Technolgies software – though at this stage I am uncertain whether or not the Polar RS800 might also yield similar information when used in conjuction with FirstBeat technolgies software ).   However, because my own personal approach is to try to understand the physiology, for the time being, I am inclined to continue to use my own amateur set-up.  With my set up I can also examine the waveform of the ECG.  I am still inclined to think that the size and shape of the T wave might be quite informative (despite the lack of clearcut conclusions subsequent to the report by Forbes and Ursula Carlile fifty years ago). However, my set-up does not allow wireless recording, so it is only useful for resting and standing measures.  I think that Suunto (when used in conjunction with Firstbeat software) is probably on the right path with assessment of autonomic nervous system function during sleep, every day activities and training.  I aim to post some more information on these issues in my blog over the next few weeks.

Additional Edit (30 June): As I explore the Firstbeat Technologies website ( http://www.firstbeat.fi/ ) I am starting to get a clearer understanding of which devices  can be used to perform the various measurements (all derived from HRV data) that have been developed by Firstbeat Technologies, which is a spin-off from the Research Institute for Olympic Sports, Jyväskylä, Finland

My current understanding is as follows:

Suunto t3 and t4 provide a ‘real time’ read out of Training Effect.

Suunto t6 with Suunto training manager software can provide more detailed analysis including Training Effect and  EPOC

It appears that Firstbeat have provided Suunto with the relevant software for incorporation in the Suunto Products.

Furthermore, I understand that data from either Suunto t6 or Polar RS800 can be read directly by Firstbeat Technologies software and used to compute Training Effect, EPOC and several other physiological variables. 

In my experience, the Firstbeat Technologies website is clear and informative, whereas I found it harder to glean the facts from either the Polar or Suunto websites.

Over-training, free radicals and HRV

Since taking up running again in middle age I have been very aware that my capacity for training appears to be greatly reduced compared to 35-40 years ago.  Once it seemed I could push the weekly mileage up to Lydiard’s recommended 100 miles per week with relatively little specific build-up.  I suspect that was because my general base fitness used to be high as a result of a range of sporting activities in childhood.  However, nowadays, if I push the weekly training volume above 55 Km per week I develop accumulating tiredness.  I have therefore been intrigued as to what it is that causes the accumulation of fatigue, and in my attempt to understand this I have explored the concept of over-training is some detail. 

Identifying over-training

The central features of over-training are relatively easy to define: accumulating fatigue, deteriorating performance, loss of motivation, a range of abnormalities of the autonomic nervous system and various biochemical and hormonal abnormalities.  However despite the range of abnormalities, it has so far proven difficult to identify a reliable laboratory test for the over-training syndrome. 

Purine metabolism and free radicals

Among the tests that make the most sense to me are tests of abnormal purine metabolites generated by the breakdown of the high energy molecule, ATP –adenosine triphosphate.  (Adenosine belongs to the goup of chemicals known as purines). In the process of releasing the energy stored in its so called ‘high energy phosphate bond’ to provide the energy for muscle contraction (and many other energy consuming processes within the body) ATP loses a phosphate group and becomes ADP  -  adenosine diphosphate .   The ADP can be re-used, but some of it gets broken down to simpler molecules and unless it is salvaged, it is excreted from the body in the form of uric acid.   The crucial issue with regard to damage to tissue is that intermediate steps in the metabolic pathway from adenosine to uric acid  result in the creation of ‘free radicals’.  Free radicals are highly reactive molecules that can cause damage by oxidation of various intra-cellular molecules.  In principle, this might happen in both heart muscle and in skeletal muscle and hence it is of potential interest to an athlete concerned about possible cumulative damage to either heart or skeletal muscle.  Free radical damage is especially likely to occur in older runners, but should not  be completely ignored by younger runners.

The fact that energy metabolism can lead to the creation of free radicals is the reason anti-oxidants have been popular among health food enthusiasts, though unfortunately there is no convincing evidence that consuming anti-oxidant supplements does any good and indeed might even do harm.  So I simply eat a sensible amount of food rich in anti-oxidants. 

This speculative relationship between purine metabolism and over-training has been given some substance by a recent study by Zielinski and colleges from Poznan in Poland (Eur J Appl Physiol May 29, 2009, Epub ahead of print). They examined levels of various metabolites of adenosine in the blood of young athletes (average age 22 years) and found substantial accumulation of these metabolites after exercise, that varied in magnitude at different phases of the training cycle.  It would be very premature to conclude that a rise in purine metabolites after exercise is a sign of over-training but nonetheless, does provide some grounds for further exploration of the idea that free radical damage may contribute to over-training, and maybe might even sometimes  result in irreversible changes. Whatever the mechanism of damage, over-training is clearly something to be avoided, by both old and young athletes. 

The central conundrum of training

The conundrum is that fitness arises via super-compensation for minor degrees of tissue damage produced by subjecting the body to stress.  Without stressing the body, and then allowing a recovery phase in which super-compensation occurs, we cannot become fit.  Optimal training requires the right balance between stress and recovery.

To a large extent we must listen to our bodies, and take things a little more easily when we experience accumulating fatigue, but it is tantalizing to ask whether or not there might be some physiological measurement to guide us.  So far no reliable biochemical or  hormonal measure has been identified and in any case, for the amateur athlete, regular laboratory testing is impractical.   However, in an era in which heart rate monitors are widely available, it has become feasible to measure the function of the autonomic nervous system, which controls many bodily functions including heart rate.

The autonomic nervous system

The autonomic nervous system governs the way in which we respond to threat or stress, and is sensitive to a very wide range of signals from within the body.  It governs short term responses such as the need to increase heart rate to deliver blood to exercising muscles, and also to ensure blood pressure is adequate to supply the brain.  But it also takes account of the body’s longer term needs, and it apparently acts to prevent us from over-exerting ourselves.  In general terms, all is well provided there is a good balance between the activity of the sympathetic nervous system, which promotes fight or flight, and the parasympathetic system which promotes relaxation and recuperation. 

However, if there is too much stress and too little opportunity for recovery, the action of the sympathetic system tends to become dominant – this leads to an over-training syndrome dominated by excessive sympathetic activity.  Potential markers for this include increased resting heart rate, an exaggeration of the normal increase of heart rate on rising from lying to standing (‘the orthostatic test’), and a loss of the high frequency variability (HRV) in heart rate, generated by parasympathetic input to the heart.

However, the body can react to cumulative stress even more dramatically by producing a excessive surge of parasympathetic activity that has the opposite effects.  When this happens acutely, the result is dizziness due to lack of blood reaching the brain, or even an outright faint.  When the excess parasympathetic activity occurs on a more sustained time scale, the result is the parasympathetic form of the over-training syndrome.  It is probable that this represents compensation by the body, possibly driven by a governor located in the inferior aspect of the frontal cortex of the brain that is responsible for regulating the parasympathetic system , to protect us from ourselves. 

The reason for laying out all these speculations is to dispel the idea that it is likely that any simple measure of heart rate or heart rate variability will prove to be a universally useful indicator of the over-training syndrome. 

1998 – a new heart rate test!

Among the FAQs on the website of Polar, the company that pioneered the manufacture of wireless heart rate monitors, is an article entitled ‘The new heart rate based test gives a pre-warning of an overtraining condition’.  This describes a test based on measuring heart rate variability on waking and after rising to maintain a standing position for several minutes. 

(http://www.polar.fi/support/faqs?product=&category=Training)

The test was developed by Dr. Arja Uusitalo, at the Research Institute for Olympic Sports in Jyväskylä, Finland.  The article on the Polar website proclaims optimistically: ‘The most demanding task for the coach and the athlete is to find out the cause of the overtraining condition and how to control it. What makes it easier, is that a new test will tell whether the condition was fatigue, caused by an acute stress situation, or an athletic burn-out as a result of too heavy training.’  The data on which that article was based was published in Dr Uusitalo’s PhD thesis in 1998.  

What has happened since 1998? 

Surely if the optimism implied by the article had been fully justified, many of us would have by now invested in an advanced Polar HRM and use this test to monitor our training.  In fact, since 1998, Dr Uusitalo, together with her colleagues from the Institute for Olympic Sports in Jyväskylä, has published a number of important articles on HRV and over-training.  The findings are only moderately supportive of the value of HRV measurements, though overall, I interpret these articles as providing support for the hypothesis that HRV is potentially a useful indicator of over-training.  However, it would be far too simplistic to expect a single test, such as that proposed by Dr Uusitalo in 1998, to provide a reliable answer in all situations.   In light of the complexity and variability of the over-training syndrome, one might predict that any test of HRV would have to be interpreted in light of individual characteristics and circumstances.

What do Polar offer in 2009?

Polar now offer a test procedure called the Own Optimizer which is based on five heart rate and heart rate variability measurements: two of the five values are calculated at rest, one while standing up and two while standing. It is not clear to me exactly what these five measurement are, though it appears likely that both the orthostatic test (change in heart rate on standing) and change in HRV on standing are included.  Unfortunately, Polar present very little evidence regarding the utility of Own Optimizer.  On the Polar discussion forum, a moderator named Mico refers to evidence from a study of  endurance training guided individually by daily heart rate variability measurements, performed by Antti Kiviniemi and colleagues from Oulu in Finland  (Eur J Appl Physiol. 101(6):743-751, 2007) [the reference given on the Polar website was not quite accurate, but this appears to be the relevant study]

Training guided by HRV

The study by Kiviniemi reports a comparison between a 4 week training program guided by HRV and a pre-defined training program   The predefined program entailed two sessions at low intensity and four at high intensity each week, for the 4 weeks.   The HRV guided  training program was based on individual changes in high-frequency HRV,  measured every morning.  If there was an increase or no change in HRV, the athlete performed high-intensity training on that day. If there was significant decrease in HRV (below reference value or a decreasing trend for 2 days), low-intensity training or rest was prescribed. 

VO2max improved significantly from 56 to 60 ml/min/Kg in the HRV guided group, but only showed a non-significant increase from 54 to 55 ml/min/Kg in the group who followed the predefined program.  Furthermore, running velocity in a treadmill test  increased by a significantly greater amount in the HRV guided group than in the predefined training group.  The authors concluded that cardio-respiratory fitness can be improved effectively by using HRV for daily training prescription.

The report by Kiviniemi is intriguing and indeed a cause for optimism.  However, it needs to be interpreted in light of the many other studies of HRV and training (or over-training) that have been published in the past decade. I will attempt to review some of the studies that I think tell an interesting story, in future postings on my blog, though at this stage, the overall conclusion is that HRV might potentially be useful  to monitor training, but no reliable simple test has yet been developed, and the data must be interpreted in light of individual circumstances.

High intensity v low intensity training for the heart

My post on 20^th June looked at the evidence  that training can produce both cardiac hypertrophy and increased blood supply to the heart muscle – the combination  of features that distinguish healthy hypertrophy for the unhealthy hypertrophy seen in some cases of cardiovascular disease.  The evidence from studies of pigs on treadmills and novice runners following a moderately demanding aerobic program is that several months of aerobic training can produce a substantial increase in the mass of the left ventricle – eg a 15% increase in mass after 6 months training in Rodriguez’s study of healthy but previously untrained young men (Am J Cardiol. 97:1089-92, 2006). This increase was associated with increased ventricular diameter and increased thickness of the muscular walls of the heart.  There was an associated increase in VO2max, a direct measure of aerobic capacity and a strong predictor of performance over middle and long distances.

Naylor’s study of elite athletes also demonstrated an increased ventricular mass after 6 months training in elite athletes (J Physiol 563; 957-963, 2005), but the increase was less than in the novices studied by Rodriguez and there was a disconcerting observation that despite pre-existing hypertrophy from previous years of training, at the beginning of the study (after a 6 week lay-off) the elite athletes had evidence of slower filling of their ventricles, which would reduce the capacity to utilize the additional muscle mass effectively.

 The contrast between the studies by Rodriguez and Naylor demonstrates that the benefits of a training program vary depending on the prior training status of the athletes.  Consequently, it is difficult to provide a clear answer to a very simple question: what form of training is likely to be most beneficial for improving cardiac function.

 The alternative to examining the results of studies of training programs is to examine what we know about the mechanism of hypertrophy.  Unfortunately, rapidly growing knowledge about the mechanisms by which the body responds to training has revealed just how complex these mechanisms are.  On account of the scope for unpredictable interactions between many variables, prediction of the final outcome on the basis of simple theory is unreliable.   My own view is that the most sensible approach is to combine what we know about mechanisms with the evidence from studies of training, and test that against one’s own experience – since  no two individuals are identical in genes and experience and therefore each person has to find out what works for him or her.

 

Speculation based on theory

First we need to ask what variable is of greatest interest.  For the middle and long distance runner, the most important demand on the heart is to deliver a large volume of blood bearing oxygen – the capacity to do this is known as cardiac output – the volume of blood delivered per minute.  This is the product of heart rate and stroke volume.  From the point of view of aerobic performance, the ultimate measure  is VO2 max, the maximum rate of utilization of oxygen. This is calculated by multiplying  cardiac output by oxygen extraction fraction.  Oxygen extraction fraction is a property of the skeletal muscles determined by capillary density and density of mitochondria in the skeletal muscle.  But for the present purpose we are concerned about training the heart.  Therefore, the trainable quantity if greatest interest for our present discussion is stroke volume.

The acute effect of ventricular filling

 Stroke volume is determined largely by the diameter of the ventricles but also by the efficiency of filling of the ventricles and the power to eject blood from the ventricles.  One of the important features of the function of cardiac muscle is the fact that stretching immediately prior to contraction produces a more powerful contraction – this is the Frank-Starling principle. As heart rate and cardiac output rise in response to demand for oxygen in the muscles, the return of blood from the periphery rises, greater stretching occurs during filling, and a more powerful contraction is produced.  In a trained athlete, stroke volume normally increases as the  cardiac output, and therefore the amount of blood returned to the heart, increases, reaching its maximum when heart rate reaches its maximum. 

In the early phases of training, increase in blood volume leads to greater filling and more powerful contraction.  Incidentally, either dehydration or the forcing of fluid into body tissues that accompanies an increase in blood pressure, decreases the volume of blood returned to the heart, so stroke volume falls and heart rate needs to rise higher to compensate to maintain a given cardiac outpt. VO2 max will be truncated because maximum heart rate does not change substantially. 

 The long term effects of ventricular filling

 Not only does increased cardiac filling promote an immediate rise in force of contraction, but the stretching of the heart muscle at the end of the filling phase (diastole) acts as a trigger to hypertrophy, apparently via the Akt signaling within the heart muscle cell, which ultimately leads to both the generation of additional contractile proteins and also the parallel development of capillaries, as discussed in my blog a few days ago.  This hypertophy will lead to an increase in both the diameter  of the ventricles and also the thickness of the walls of the ventricles, as demonstrated in the study by Rodrigues et al (Am J Cardiol. 97:1089-92, 2006).

So the most efficient form of training for increasing stroke volume and for the associated development of capillaries supplying the heart muscle is likely to be fairly vigorous exercise that produces a large amount of filling of the ventricles during diastole.  It would be expected that the  greatest benefit per unit of time spent training will be gained by training near VO2 max – though of course the overall picture must take into account the risks  associated with training at this level.  We will return to that issue again in the future.

The myoglobin effect

However one additional point needs to be made. If training is to be above the lactate threshold, then each effortful interval must be relatively brief – but not too brief, because of the phenomenon of buffering by myoglobin. At the beginning of an effortful interval, oxygen attached to myoglobin in the muscles can meet the metabolic needs for a period of a minute or so, so the demand for cardiac output does not reach a peak until about two minutes after the start of the effort.  Therefore, one might expect that intervals of three or four minutes duration would proved the best value for time spent (though alternatively one might do shorter intervals if the rest period is very short (eg 10-20 sec) so that myoglobin is only partially  replenished during the rest period).

 Matching observation to theory

How does observation match theory?  There are very few studies that have directly compared the changes in stroke volume after a program of high intensity interval training compared with lower intensity aerobic training. The only one I know of is by Helgerud and colleagues from Trondheim in Norway (Med Sci Sports Exerc. 39(4):665-71; 2007). They randomly allocated 40 moderately trained male participants (with initial VO2 max around 60 ml/min/kg)  to one of four training groups for 3 sessions per week for 8 weeks:

 1) long slow distance (LSD) (70% maximal heart rate);

2) lactate threshold (85% HRmax);

 3) 15:15 interval running (15 s of running at 90-95% HRmax followed by 15 s of active resting at 70% HRmax); a session included 47 x15 s effort intervals.

4) 4 x 4 min of interval running (4 min of running at 90-95% HRmax followed by 3 min of active resting at 70%HRmax).  

The amount of work in each session was adjusted to that the total oxygen consumption was similar is all four groups. 

The two interval training programs resulted in a significantly greater improvement of VO2max (5.5% for 15:15 and 7.2% for 4 x 4 min intervals than the low intensity aerobic and lactate threshold sessions. Furthermore stroke volume increased by approximately 10%  after each of the high intensity interval programs.  Thus, it appears that compared with low intensity aerobic or lactate threshold training, high intensity interval training produces greater improvements in VO2 max  and parallel increases in stroke volume, in accord with expectation based on theoretical considerations.

 High intensity is best, but in moderation

Thus the most efficient from of training for producing an increase in stroke volume and VO2 max appears to be high intenirty interval training.   This certainly does not mean that a training program should consist entirely of high intensity sessions for two reasons.  First, it is necessary to take account of the need to train the leg muslces as well. Increasing capillaries and mitochondria in leg muscles, and also developing the ability to withstand eccentric contractions of the leg muscles for the duration of the intended race are also important aspects of optimizing racing performance.  At least for long races (half-marathon and marathon) training the leg muscles to cope with multiply repeated eccentric contractions at each footfall is crucial, and this requires a substantial training volume.  The second issue is avoiding too much stress on the heart.  The crucial issue here is maintaining heart rate variability (HRV).  HRV can be improved by training, but both excessive volume and excessive intensity of training can impair HRV.  I will examine this issue in more detail in my next posting.

 Nonetheless the simple conclusion with regard to increasing cardiac output is that both medium intensity aerobic training (as employed in the study by Rodriguez, considered in my post on 20^th June) and high intensity interval training can produce benefits, but high intensity interval training is the more efficient.

Furman re-visited

In March I had set myself the goal of running a half marathon in 99 min in the autumn.  In my blog postings around that time, I looked into the potential advantages and disadvantages of the Furman training program: a relatively low volume, high intensity program that consists of three running sessions per week – a long run a tempo run and an interval session, all to be run at predetermined paces based on target race pace, together with several cross training sessions. 

 

At that stage I still had time for some additional base-building before embarking on a program focused on the half-marathon.  With my intended race now little over three months away, it is time to make a definite decision.  I continue to be tempted by two aspects of the Furman program: the fact that it requires only three running sessions per week augmented by cross-training, and the fact that I enjoy the sensation of running at moderately fast paces.  So to help me decide, I have looked into the evidence from two sources: information gleaned from the experiences of other bloggers who have followed the Furman program; and a review of the progress I have made during the past three month of base-building.

 

The experiences of other bloggers

I sporadically follow the blogs of a number of runners whom I would describe as dedicated amateurs: amateurs in the sense that they appear to run mainly for the love of running; dedicated in the sense that train regularly while meeting the demands of a regular job and/or family.  In recent months, I have kept an eye out for dedicated amateurs who have committed themselves to the Furman program.  In fact I have come across only two such bloggers.  Maybe this is itself tells us something, as there appear to be substantially more blogs describing programs that might be described as Lydiard-style programs.  Nonetheless, the two individuals have interesting stories to tell.  It would be unwise to draw too many conclusions from only two accounts, but the advantage of the stories of individuals is that one can assemble a richer picture of the background fitness and other individual factors that get lost in the reports of scientific studies.

 

I am not sure about the etiquette of quoting from other people’s blogs about themselves, but assume that if they have put the material in the public domain that they are happy for others to try to learn from their experiences. You can read their own accounts to get the facts; any conclusions I draw say more about me than about than about them.  Nonetheless, I will let both individuals know that I have mentioned them so they can correct any misperceptions if they wish. I would also be delighted to hear from anyone else who has tried the Furman program.

 

Charlie

http://runningnowherefast.blogspot.com/2007/08/furman-first-to-finish-program.html Charlie adopted the Furman program to prepare for the Marine Corp Marathon (in Washington DC) in October 2007. At time he was a 52 year old who had been running off and on since high school, but had begun to take running more seriously recently.  In April 2007 he had run a half marathon in 1:32:26, and a 10K in 41:58:55.  His usual training program included a large amount of cross training, including use of elliptical, stair-stepper and swimming.  He set his Furman training paces according to a planned marathon pace of 7:20 min per mile which corresponds to 3:12:00 for the marathon.  He started at the 4^th week of the 16 week Furman marathon program but at that stage had already been training hard for 5 weeks. Here is a description of the final stages of his first Furman session, a 5×1Km interval session at 5:53 min per mile  pace (3:40 /Km), following a rest day:

‘I could barely finish the fourth one…leaving me gasping for air and taking a minute more for my RI. For the fifth one I dropped the speed down to 10 mph [6 min/mile] and barely finished that one…thankful the series was over. 

However he found the 20 mile long run that week easy and couldn’t restrain himself from increasing the pace from the planned 8 min/mile to an average of 7:15 min/mile for last 2 miles.  At the end of the week he concluded

‘My first week of the Furman program is under my belt. I found the speed intervals was my hardest day and the other two days were fairly easy.’

As he progressed through the program he continued to find the speed interval sessions hard but coped well with the other sessions.  On race day, he covered the first half of the marathon in 1:37:38, but a few miles later he developed muscle cramps and struggled to finish in 3:47:28, a very respectable performance but well short of his target.  Only two weeks later, on 11 November he entered the Richmond Marathon. He started more slowly and did the first half in 1:41:10.  This time he did not suffer cramps during the second half, and finished in the creditable time of 3:23:26, in fact a really impressive performance only two weeks after his travails in the MCM.    

So in his marathon campaign in 2007 Charlie did very well, but fell a little short of the potential indicated by his half marathon and 10K times recorded in April.  I would anticipate that a runner with a half marathon time of 1:32:26 and with legs optimally prepared for the rigors of the longer race, would be capable of a marathon in the range 3:12:00 to 3:15:00. It plausible that a larger number of long training sessions run at a less punishing pace might have resulted in better conditioning of his leg muscles, though whether or not that conditioning could be achieved in a single season by any training regimen is doubtful.     

 

Paul

http://2009marathoncampaign.blogspot.com/

The other ‘dedicated amateur’ blogger who used the Furman program is Paul.  I discovered his blog as a result of a comment he left on my blog, reporting the outcome of his recent run in the Sri Chinmoy half-marathon in Williamstown (Melbourne).  Paul is a forty year old triathlete who had run a half-marathon in 97 minutes about 15 years ago, and in February 2009, initiated his campaign to prepare for the Melbourne marathon in October.  In the first week of his campaign he completed a 500m-20km-5km. triathlon in 1:15.43, running the final 5Km in 23.:29.  Thus, at that stage he appeared to have the speed and endurance to run a half-marathon in around 98-99 minutes.  He confirmed this potential with a 10K in mid-March in 44:54, which according to the Daniels VDOT tables, corresponds to a half-marathon time of 98:30.     

At the end of March he commenced the Furman half-marathon program, starting 10 weeks out from his interim target of a half-marathon at the end May.  This is what he wrote after his first session:

‘This is hard!!! I had to complete 2x 1.5km easy (5.28min/km) and 3.5km tempo (4.38min/km) with a cool-down so a total session of 11km. I found pacing pretty hard to set and ended up running a little faster on the easy bits (7.47 and 7.56) and a little slower on the tempo sets (16.21 and 16.48).’

He didn’t find the first long run of the program any easier.  A few days later he wrote:

‘Crikey, that was a hard run today! I knew this program wouldn’t be easy, but I didn’t realise I’d find it so hard from the start.   Somewhere along the course today I realised that this program says Run #3 each week is a long run. It does not say it is an EASY long run. … In any case today was a 13km run at HMP (Half Marathon Pace) +12 sec/km…But, managed to run 63.54min against a target of 63.42min so essentially right there. But it was no gentle Sunday morning stroll.’  

However, as the weeks went by Paul started to find the long runs easier, and by the end of the program was comfortably completing the long runs at a pace around 4: 53 per Km.  He went on to record 1:33 in the Sri Chinmoy half-marathon on May 31^st.  He will soon be starting the Furman marathon program.  So, my interim conclusion from Paul’s experience is that for a runner with a sound base, the Furman half-marathon program is tough, but can produce a spectacular improvement 

A review of my own situation

In my younger days I used to enjoy the sensation of running at a moderately fast pace.  During my brief return to regular running during my fifties I had been a little frustrated by the fact that I was no longer able to run fast, but nonetheless had started to get the sense that it might again be possible, as my pace for tempo runs decreased to around 4:30 min/Km.  Then an exacerbation of my long standing asthma and also the demands of work led me to stop running for about 18 months.  On realizing how unfit I was becoming I restarted running again in 2007, but progress has been slow.  

For two years I trained mainly at fairly low intensity, rarely covering more than 50Km in a week, and averaging around 35 Km per week.  In September of both 2007 and 2008 I had run a half-marathon, on each occasion recording a time of 101:xx minutes.  I decided that this year I would make a more determined effort to increase training intensity and have set myself the goal of a half-marathon in 99 minutes in the coming September.

When I reviewed the options for a training plan in March, I had weighed up the merits of either a Lydiard-style relatively high volume program or a Furman high intensity program.  I realized that I did not have an adequate fitness base to enable me to tackle the Furman recommended training paces, especially the recommended pace for the majority of the long runs (half-marathon pace + 12 sec /Km) .  For a target half-marathon time of 99 min the recommended long run pace is 4:54 min/Km.  I therefore decided to defer the decision until after I had spent a further 10-12 weeks building up my fitness base.  As stated above, now is the time to make the decision.

In the past three months, my asthma has continued to be an intermittent problem, leading to mild wheeziness and a 35-45 % fall in expiratory flow rate after a vigorous training session.  Furthermore, the fact that I often arrive home from work after 8pm in the evening, tired and hungry, has curtailed my plans to do really solid base building.  The mainstay of my training has been back-to back moderately long runs in the lower aerobic zone on the week ends, with several short evening sessions during the week.  Typically I have done one session of uphill strides; a fartlek run of 6-8 km; an easy run with some alactic sprints and an elliptical cross-training session most weeks.  I have averaged a little over 50 Km per week.  During this time my aerobic fitness has continued to improve slowly.  

As I have mentioned previously on my blog, I find that heart beats per Km for runs in the aerobic zone over easy terrain when not stressed is a fairly consistent indicator of my aerobic fitness.  When I recommenced training in 2007, my score on this measure was over 800 beats/km, by February 2009 it was around 700 beats/km and now it is typically 650-660 beats/Km.  I estimate that a value of 645 beats/Km would represent adequate aerobic fitness for a 99 min half marathon.   On my current training schedule, I would anticipate achieving this level by September, so there is little reason to change my current schedule for the purpose of increasing aerobic fitness.

However, the other main requirement for achieving my half-marathon target is conditioning my leg muscles to cope with a pace of 4:42 min/Km for 21Km without substantial muscle damage.  How near am I to achieving that goal?  My back-to back longish runs on the week-ends have demonstrated that I can fairly easily maintain a pace around 6 min/Km for 20Km.  Yesterday (Saturday) I decided that I would test my ability to increase the pace during a 16Km run.

Unfortunately, as is often the case, I had had a busy week at work and I felt very lethargic as I warmed up.  Even after a few stride-outs over distances of 50-150 metres I still felt very sluggish.  So I decided that the most practical thing was to start at a pace of around 5:10 min/Km, which I anticipated would be in the lower aerobic zone, and increase pace steadily with the hope of reaching and maintaining the my intended half-marathon pace over the final few Km.

I covered the first 4Km in around 20:30, with a heart rate in the lower aerobic zone as expected.  I continued to feel sluggish but nonetheless enjoyed the sensation of gradually increasing my pace.  With 4 Km to go my legs still felt heavy but I was by now near to my intended race pace and really enjoying feeling of running faster.  I covered the final 4Km in 18:48 min (4:42 min/Km), which was exactly my target pace.  My time for the 16Km was 80 minutes and mean heart rate 130 beats/min, corresponding to 650 beats/Km.  Although my average pace was modest, this run clearly extracted a price from my muscles. I awoke with appreciable stiffness in my leg muscles, and during an easy 8Km recovery run, my heart rate was 696 beats/Km.  Experience has taught me that an increase of this magnitude indicates a moderate degree of over-reaching.  If I take it easy tomorrow I expect that I will have recovered completely by Tuesday.

So what conclusions should I draw?  I am fairly confident that irrespective of the specific training strategy I adopt, provided I continue to train regularly for the next three months, my aerobic fitness (i.e capacity to deliver oxygen to my muscles at the required rate) will be adequate to allow me to achieve my target half-marathon pace while remaining within the aerobic zone.  However my leg muscles are still far from adequately conditioned for the task of maintaining this pace for the required distance.  The two ingredients missing from my recent program are tempo runs in the upper aerobic zone, and longish runs (around 16 Km) at a pace not far below race pace. 

The tempo sessions and fast longish runs might be provided by the Furman program.  However, I do not anticipate the demands my job becoming any less in the next few months, and I do not relish the prospect of fitting two very demanding midweek sessions into my current work schedule.  Furthermore, I do not want to abandon my current back-to-back longish runs on weekends entirely, as I think these runs have served me well so far.   Therefore, I think it is probably more practical to continue with a weekly program that includes 5 or 6 running sessions, including at least one tempo run and a hill session each week, and longer runs on the weekend that alternate from week to week.  One week I will do a fairly fast run of around 16Km (aiming for the Furman recommended long run pace of 4:54 min/Km)  and the following weekend I will do back-to-back  longer runs in the lower aerobic zone. 

Maybe this medium intensity/medium volume plan is neither fish nor fowl, but I think it will more enjoyable than a rigid Furman schedule and I suspect it will be adequate to allow me to achieve my goal this year.

Re-examining the components of base building

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.

 

Aftermath

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

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 ( http://swingleydev.com/misc/exercise.php ). 

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

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 8×1Km 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.

The path to fitness or to over-training

The path to fitness

Successful training is based on a delicate balance between stressing the body and allowing it to recover. In the short term stress leads to damage and impaired performance but provided there is adequate opportunity for recovery, the body’s response to the challenge is to not only repair the damage but to develop a greater capacity to withstand challenge in future. This is described as super-compensation but in everyday terms, it simply means the body becomes fitter.

The path to over-training

However, if there is inadequate opportunity for recovery, performance continues to deteriorate and the body enters a state of staleness described as overtraining, that can persist for many months. In the over-trained state many aspects of body physiology are prone to be disrupted though there is no single physiological measure that indicates over-training. It is probable that the processes that lead to overtraining involve local trauma to body tissues, excessive production of ‘stress’ hormones such as cortisol, and excessive production of other chemical messengers in the body such as cytokines that re-set the brain mechanisms that regulate the body. It is probable that the derangements of body chemistry in any one case depend on the nature of the initial stress; on the genetic constitution of the individual; and on that individual’s previous history of stress and adaptation.

The first steps on the path to fitness or over-training

For long-distance runners, there are two processes that are the most likely candidates for initiating the processes that lead to either fitness or overtraining. These are damage to muscle fibres produced by the eccentric contraction that occurs on each footfall, and the release of cortisol by the adrenal gland to promote the generation of glucose required to fuel a long run. Understanding these processes is likely to be the key to rationally designing a successful training program.

Catabolic effects of cortisol

When the body faces stress, the initial response is release of cortisol from the adrenal gland. Cortisol plays part in several of the body’s immediate self-protective strategies. Of particular relevance for the long distance runner is the process of gluconeogenesis – the generation of glucose to prevent a fall in blood glucose that would be a catastrophe for the brain, which is heavily reliant on glucose to fuel its operations. Cortisol promotes the release of glucose from glycogen stores in the liver. However cortisol can also promote the breakdown of protein to generate glucose. So unaccustomed long runs are likely to result in the sacrifice of muscle protein for the sake the short term maintenance of blood glucose. This breaking down of body constituents is known as catabolism.

Eccentric damage to muscles

The mechanisms of muscle damage during exercise are not fully understood. It is unlikely that processes such as lactic acid production due to anaerobic metabolism play a significant role. It might be that increased acidity interferes to a limited extent with some beneficial processes such as the generation of mitochondria, (as indicated by the study by David Bishop and colleagues (Medicine & Science in Sports & Exercise:Vol 40(5) Supplement p S33, 2008), discussed in my post on 21st April. However, a substantial amount of evidence indicates that lactate actually protects muscles (Cairns SP, Sports Med. Vol. 36(4):279-91, 2006) Another potential mechanism of damage is the production of free radicals,. These are reactive molecules with an unpaired electron that are formed during oxidative metabolism and can damage tissue, but so far the evidence suggests that free radical damage is on likely to be a serious issue for elderly runners. (I myself am in that group, but in the present discussion I do not want to confine myself to the challenges facing the elderly).

As discussed above, the catabolic effects of cortisol can also promote break-down of muscle. However, the most significant source of damage during running is likely to be simple mechanical trauma. During weight lifting, the eccentric activity involved in controlled lowering of the weight can produce dramatic disruption of the structural integrity of muscles, that far exceeds the damage caused during concentric lifting, even though concentric lifting requires more energy. Forcefully stretching a muscle as it is actively generating an opposing force simply tears many of the muscle fibres apart, producing the pattern known as Z-line streaming (Gibala and colleagues, Journal of Applied Physiology, Vol 78, 702-708, 1995). Unfortunately, eccentric contraction occurs at each footfall during running, as the quads and calf muscles arrest the freefall under the influence of gravity that occurred during the airborne phase. Thus long distance running produces two potentially destructive effects: micro-trauma that tears the muscle fibres apart and the release of the catabolic hormone, cortisol, which acts in the short term to maintain blood glucose levels, but when the supply of glycogen in the lever is inadequate, is likely to breakdown muscle proteins to generate glucose. In the short term, muscle power suffers but in the medium term, these destructive processes can trigger adaptive responses that lead to greater fitness – provided the stress is not excessive. On the other hand, rapid increases in training volume leads to over-training and possible long term impairment of function, as was illustrated ib the study by Lehmann and colleagues discussed in my posting on 14th April (Int J Sports Med. Vol 12(5):pp 444-52, 1991; Br J Sports Med. Vol 26(4):pp 233-42, 1992; Eur J Appl Physiol Occup Physiol. Vol 70(5):pp 457-61, 1995).

The adaptive response to muscle damage

Several adaptive processes can occur. The two most important are closely linked: these are the mobilization of satellite cells and the production of anabolic hormones. Satellite cells are a form of stem cell that occur in muscle adjacent to the muscle fibrils. Following damage to the muscle, the satellite cells fuse with the muscle cells ( GE Adams, Satellite cell proliferation and skeletal muscle hypertrophy, Appl Physiol Nutr Metab. Vol 31, pp782-790, 2006). Muscle cells have multiple nuclei, containing the DNA and other molecular machinery necessary for initiating the synthesis of new proteins. When a satellite cell fuses with a muscle cell, it adds a new nucleus thereby enhancing the regenerative capacity.

Corticosteroid hormones can inhibit the action of satellite cells. This is most clearly established in the case of synthetic steroids such as prenisolone that are used for the treatment of autoimmune disorders (Betters and colleagues, Muscle & Nerve. Vol 37(2):pp 203-9, 2008). However, it would be expected that less potent naturally produced corticosteroids such as cortisol would have a similar, though perhaps less marked effect.

However, the hormonal regulation of metabolism entails not only the production of catabolic hormones such as cortisol that tend to break down body tissues, but also the production of anabolic hormones that promote the building up of body tissues. The most potent of these are the sex steroids, especially testosterone (though oestrogen also has anabolic effects). Vigorous muscular contraction promotes the release of testosterone (Grandys and colleagues, J Physiol Pharmacol. Vol 59 Suppl 7:89-103, 2008). Testosterone promotes the action of satellite cells.

The adrenal cortex also produces anabolic hormones of which DHEA (dihydroepiandrosterone) is the most abundant. DHEA is a multifunctional hormone, and its role in adaptation to training is uncertain. The question of whether DHEA supplements have a beneficial effect on muscle building has been a subject of some controversy. Less controversial are the beneficial anabolic effects of growth hormone. Growth hormone is produced by the pituitary gland and stimulates the building up of body tissues. The production of growth hormone is promoted by vigorous exercise, but the peak release of growth hormone occurs during sleep. Almost certainly, adequate sleep is required to promote the optimum switch from production of the catabolic hormone cortisol (which usually reaches its lowest level 3-5 hours after onset of sleep) to the production of growth hormone.

Failure of adaptation

If the amount of time for recovery is inadequate to allow the repair of muscle fibres and the re-synthesis of glycogen, a vicious cycle sets in. The damaged muscle tissue release cytokines which are small molecules that carry out various signaling functions in the body. Although the details remain speculative, it is likely that the cytokines produced by muscle damage act in the hypothalamus and in other regions of the brain to re-set the regulatory mechanisms that control the various physiological processes in the body (Smith LL,.J Strength Cond Res. Vol. 18(1):pp 185-93, 2004). In particular, the regulatory mechanisms are likely to shut down body functions that might promote further damage. In other words, your brain will not allow you to run far or fast. Cortisol production initially remains high, though eventually it is likely to fail. Anabolic steroid production falls. You will feel stale, de-motivated and possibly even depressed. You are now over-trained and it may be many months before your brain lets you engage in potentially destructive activities such as racing at your best level.

What are the lessons?

This brief (and somewhat speculative) exploration of modern molecular biology confirms what has been discovered by observant athletes and coaches over the years. The simplistic explanations such as the presumed damaging effects of lactate suggested by coaches such as Arthur Lydiard are probably wrong, but many of Lydiard’s observations of what works in practice are probably correct. However a thorough understanding of the molecular biology might allow a somewhat more effective application of the principles.

A few specific points that might be gleaned from the discussion above are:

1) long training runs are potentially beneficial as they provide an enough stress to produce appreciable muscle damage and appreciable cortisol production.

2) Rapid increase in training volume is likely to lead to over-training. On the other hand, if the build up of training volume occurs slowly, the adaptive processes will result in an increased capacity to cope with the stress of heavier training and in turn, to reap greater benefits.

3) Cross training employing a training mode that minimizes eccentric contractions (e.g. elliptical cross training; cycling or swimming) will allow a greater total training load at any given level of fitness, and in particular, might facilitate other valuable adaptations (e.g. increase in blood volume; increased cardiac stroke volume; increased ability to generate glucose from lactate in the liver) without triggering the cytokines that signal to the brain that it further training should be inhibited.

4) Adequate periods of recovery are essential and in particular, adequate sleep is crucial during period of heavy training.

Risks of increasing volume v increasing intensity

In my recent post on base-building, muscle damage and adaptation, I had reported evidence demonstrating that there is are multiple paths to success in training.  Both anecdotal evidence about the training of world record holders and also the evidence from scientific studies suggest that both high volume programs and also high intensity programs can produce an increase in aerobic fitness and enhance performance. 

 

On the other hand, I also suggested that there are likely to be multiple paths to stunted growth, frustration or outright failure.  My own experience and also the comments of Rick and Ewen in response to that posting, suggest that the risks of ‘stunted growth, frustration and outright failure’ might be greater with high intensity training.  Certainly my own experience confirms that an increase in training intensity increases the risk of overt muscle injuriy.

 

A study of training and over-training

However, it is salutary to examine the results of the study which I regard as perhaps the most thorough comparison of the risks associated with a major increase in training volume, with the risks associated with a major increase in training intensity.  This was a study conducted almost 20 years ago by Lehmann and colleagues at the University Hospital of Freiberg and reported in a series of papers published in the 1990’s.  (The key papers are:  Int J Sports Med. Vol 12(5):pp 444-52, 1991; Br J Sports Med. Vol 26(4):pp 233-42, 1992; Eur J Appl Physiol Occup Physiol. Vol 70(5):pp 457-61, 1995).

 

The ITV and ITI programs

It should be noted at the outset that the intention of the investigators was to induce over-training, so the training regimes should not be regarded as typical of sensible training programs.  In the first year, 8 experienced middle or long distance runners took part in a brief Increased Training Volume (ITV) program that entailed a 101% increase is training volume over a three week period, from a baseline of 85.9 Km in week 1, up to 176.6 km in week 4.  Training occurred on 6 days per week.  Virtually all of this training (96-98% of training volume) was performed as long-distance runs at an estimated mean oxygen utilization at 67% of maximum capacity.   This pace corresponds quite closely to Molvar’s interpretation of Lydiard’s 1/4 effort. A year later, 9 experience runners (including 7 of those who took part in the ITV program in the first year) took part in an Increased Training Intensity (ITI) program.  Speed endurance, high-speed and interval runs averaging 9 km at baseline in week 1, increased to 22.7 km in week 4, and the total volume increased from 61.6 to 84.7 km, during ITI.  Thus both programs might be regarded as injudicious, but nonetheless, provide the chance to compare the results of injudicious increase in volume with the results of what appears to be at least an equally injudicious increase in intensity, in almost exactly the same group of athletes a year later.

 

The consequences of increased volume

During the increased volume program, there was stagnation in endurance performance capacity (running velocity at the aerobic-anaerobic transition range – a key indicator of middle and long distance performance) together with a decrease in maximum working capacity in 6, and a stagnation in 2 of the 8 runners.  Total running distance during an incremental treadmill test decreased from 4719 +/- 912 m to 4361 + /-788 m.  There was an increase in levels of creatine phosphokinase (a marker of muscle damage) and a decrease in neuromuscular excitability (which the investigators regard as a peripheral measure of good muscle function rather than a measure of neural signaling from the brain).  In the subsequent competitive season, these athletes failed to reach their previous personal best levels.

 

The consequences of increased intensity

In contrast, during the increased intensity program a year later, performance at the aerobic-anaerobic transition (i,e. at lactate level 4 mmol) and also total running distance during the incremental treadmill test improved steadily during the 4 weeks, and there was no significant evidence of muscle damage.

 

Conclusions

This study does not prove that judicious high volume training is dangerous.  However it does demonstrate that increasing training volume by around 33% per week for three weeks,at moderate aerobic paces (well short of lactate threshold) has a very high probability of producing muscle damage and reduced performance, both during treadmill testing and during the subsequent competitive season. 

 

The failure to improve performance in competition cannot be attributed to the athletes having already reached their peak, as an increase in high intensity training the following year, which at first sight appeared even more injudicious, resulted in a steady improvement in performance.  This improvement during high intensity training in experienced runners would of course be very unlikely to have occurred in novice runners.  It is almost certain that all of the runners recruited to this study already had a substantial aerobic base before entering the study. 

 

For runners who already have at least a moderate aerobic base, a ‘crash program’ of high intensity training might be expected to produce greater improvement in performance and less risk of damage, than a ‘crash program’ of increased volume.  The benefits of high volume training are more likely to come from a sustained, long-term program.