Archive for June, 2009

Should you buy a HRM that measures HRV?

June 30, 2009

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 28th 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.

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. 

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

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 ( ) 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

June 29, 2009

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. 


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.

Heart rate variability

June 26, 2009

Heart rate variability, as the name implies, is variability in the duration between consecutive beats.  In the ECG, it is variability in the time interval between consecutive R waves in the QRS complex that represents the electrical events of ventricular contraction.  In general, the heart beats faster during inspiration and more slowly during expiration.  These variations are governed by the autonomic nervous system, which is responsible for the regulation of many of the body’s internal organs and in particular, coordinates the fight-or-flight reactions that prepare our body to deal with challenging situations.  There are two distinct divisions of the autonomic systems: the sympathetic system which tends to accelerate the heart and the parasympathetic system which produces deceleration. 

Almost certainly HRV is a crucial importance to the athlete, though the details are still a subject of debate.  There are three main issues:   1) loss of HRV  is potentially a useful indicator of the stress associated with training, and there is evidence suggesting that adjusting training schedules according to changes on HRV can increase the quality of the training and diminish the risk of over-training; 2) loss of HRV is a fairly reliable indicator of sudden cardiac death in individuals with heart disease and some evidence indicates that it has similar implications even when there is no other evidence of heart disease; 3) a resilient heart with high HRV might in fact function more efficiently and hence improved HRV might itself contribute to improved performance.   In the next few posts I will attempt to examine all three of these issues, and also to address the question of how HRV might best be increased by training.

Before examining the evidence that training might have either beneficial or deleterious effects on HRV, I decided  to look at HRV in my own heart.  Both Polar and Suunto manufacture hear rate monitoring equipment that provides an estimate of HRV, but I am still undecided about the value of investing in such equipment.   Furthermore, I thought it would be interesting to examine not only heart rate variability, but also the shape of the various peaks and troughs that make up the ECG.  I rigged up a system with a lead attached to each forearm, and fed the signal to some electrically isolated amplifiers, before digitizing it so that I could subject it to some detailed analyses. (Isolation of the amplifiers is crucial for safety).  The trace recorded with this ad hoc system in not a clinical ECG, but nonetheless corresponds quite closely to lead 1 in a clinical 12 lead ECG.  Lead 1 represents the difference in voltage between left and right arms.



The ECG reflects the flow of the electrical currents that produces contraction of the heart muscle.  The current flow produces currents in the surrounding body tissues and provides a signal detectable on the body surface.  The magnitude and average direction of the current flow determines the size and shape of the various peaks in the ECG.  For our present purposes, the feature of greatest important is the rhythm, and in particular, the variability of the interval between beats.  However, a substantial number of athletes have minor abnormalities of the shape of the waveform.  Follow-up studies indicate that these abnormities are generally benign and do not create a high risk of heart attack, though the issue of distinguishing clearly between normal variation seen in athletes and pathological variation is still a somewhat vexed question.  Therefore, I was interested to examine the waveform to see whether or not I have significant abnormalities.  I am an amateur in the interpretation of ECG’s, so if a cardiologist happens to read this, I would be delighted to hear whether or not I have interpreted things correctly. 

ECG and inter-beat interval

ECG and inter-beat interval

The figure on the left shows the ECG during two successive heart beats, while the figure on the right shows the variation in inter-beat interval over a period of about 80 seconds.  The waveform looks fairly normal to me (as an amateur). 

Atrial contraction

The P wave reflects spread of the electrical signal from its generation at the sinoatrial node, though the walls of the right and left atria, and in my recording is about 80 milliseconds wide and has a height of 0.08 mV.  After an interval of around 195 millisec, the P wave is followed by a QRS complex.  The PR interval is the time between sino-atrial node firing and the firing of the AV-node which initiates ventricular contraction.  It is an important indicator of transmission of the electrical signal from atria to ventricles. The normal value is around 200ms.  Very short values might indicate a potentially serious conduction abnormality known as the Wolfe-Parkinson-White syndrome, while long values might indicate blockage of transmission, so it is reassuring that the duration of my PR interval seem fairly normal.   Between P wave and QRS complex the trace should be fairly flat, though in my case there is a slight downwards slope.  I do not know if this has any significance. 

Ventricular contraction

The QRS complex reflects the spread of the electrical signal that causes depolarization of the muscle in the walls of the ventricles.  The depolarization of the muscle cell membrane produces the muscular contraction that ejects the blood from the ventricles.  The negative Q wave represents the spread of electrical signal downwards and left-wards to the apex of the heart and the large Q wave reflects the spread around the lateral walls upwards and predominantly rightwards from the apex. In some leads of the ECG, R is followed by a small negative deflection known as the S wave, though due to the direction of current flow at this time, the S wave often small in lead 1, and in my ECG, it is scarcely discernible at all.    In a healthy heart the width of the QRS complex should be less than 120 ms.  In my case it is only about 60 ms.

Ventricular repolarization

The final peak of interest is the T wave, a hump occurring about 350 ms after the end of the QRS complex in my trace.  This denotes re-polarization of the heart muscle, making it ready to contract again.  Prolongation of the QT interval occurs in a number of pathological conditions and can also be an unintended side effect of various medications. Because it tends to be shorter at high heart rates, it is usual to estimate a corrected value known as QTc which allows for variation in the heart rate.  In my recording QTc is about 300 ms.  The usual value is around 420 ms, so I do not have any evidence of a pathologically long QTc.

One feature that is of great clinical importance is the ST segment.  This is depressed when the heart muscle is deprived of oxygen and can be elevated once the heart muscle has been damaged.  The ST segment should be flat, but in my case it rises steadily for about 100 ms preceding T wave.  As far as I am aware, this upward slope of the ST segment is quite common in athletes, and possibly denotes thickening of the ventricle walls.  The point at which ST elevation of depression is usually measured is 60 millisec after the end of the QRS complex.  At this point, my trace shows no evidence of either depression of elevation, so I am inclined to interpret this picture as indicating a healthy though perhaps slightly hypertrophic heart.


Now to the important issue for our present discussion.  My average heart rate during this recording was 46 beats per minute, which I think  is fairly typical of a fit athlete when sitting down, trying the relax but nonetheless, with my mind focused on making sure the equipment is continuing to function.  However even more striking is the variation of the heart rate.  As can be seen from the right hand figure, over the course of about 80 seconds the inter-beat interval varied from 1.1 sec (HR 54 bpm) to 1.5 sec (HR 40 bpm).  The normal variability in beat-to-beat interval is less than 10%.  So I definitely have substantially increased heart rate variability.

Even  more interesting is the time-scale of the variation. It can be seen from the right hand figure, that the dominant fluctuation are rapid (ie high frequency) fluctuation occurring on a time is around 2-4 beats (i.e over a period of 4 seconds corresponding to a frequency of  0.25 cycles/sec.)  These high frequency fluctuations are characteristic of the parasympathetic nervous system, which in general is associated with relaxation and recovery. 

However, closer inspection also reveals underlying variation on a time scale of around 30-40 beats (40-50 seconds) corresponding to a frequency of 0.02 cycles per second.  Slow fluctuations on this time scale are characteristic the action of the sympathetic nervous system – the part of the autonomic nervous system that promotes fight or flight.  So I am encouraged to observe evidence of a balance between parasympathetic and sympathetic activity, but with a particularly strong parasympathetic component.


Sympathetic-parasympathetic balance: the Poincare plot

There is an intriguing though somewhat complex way of quantifying the relative contributions of parasympathetic and sympathetic nervous system to hear rate variability, known as the Poincare plot.  The Poincare plot is a scatter plot in which each heart beat is represented by a point in a two dimensional plane, with the value of the  inter-beat interval preceding that beat is plotted on the horizontal axis and the value of the following  inter-beat interval on the vertical axis.   This scatter plot is shown on the figure below, for the same data as is shown in the figure above.  The points look a bit like a swarm of bees scattered around a line that runs diagonally upwards at 45 degrees. 

Sympathetic - parasympathetic balance: the Poincare plot

Sympathetic - parasympathetic balance: the Poincare plot


The interpretation requires some concentrated thinking but is worth the effort.  Imagine that the heart rate variability is produced entirely by sympathetic nervous system activity.  Such fluctuations occur on a slow time scale – typically varying substantially over a period  40 beats or more. Therefore for consecutive beats, the inter-beat interval is almost unchanged.  The points representing those near identically spaced consecutive heart beats must lie near the 45 degree line.  However, if there is a slow drift in values of inter-beat interval over time, due to fluctuation in the input from the sympathetic nervous system, then the points will wander up and down the 45 degree line.

On the other hand, if the fluctuations are driven by the parasympathetic nervous system, they occur on a time scale of a few beats, and the beat by beat variation will be large.  Therefore many heart beats will be represented by points that lie far away from the 45 degree line

If we draw an ellipse that is just large enough to include most of the heart beats (allowing that there will usually be few outliers that buck the general trend) then this ellipse will have one  axis pointing along the 45 degree line and the other axis at right angles to this.  The length of the axis along the 45 degree line represents the amount of sympathetic drive and the length axis at right angles to this represents parasympathetic drive. 

In individuals a high risk of heart attack the ellipse is a long thin cigar shape lying along the 45 degree line.  For individuals with a good balance between parasympathetic and sympathetic input, the ellipse is almost round. I was delighted to find that for me, the ellipse is fat and almost round.



So in summary, I am quite pleased with what my little experiment showed.  As far as I can tell, the shape of my ECG trace is near normal, apart from the upward slope of the ST segment that I understand is relatively common in athletes.  My heart rate is slow, but even more importantly, there is a large variability, driven by a good balance between parasympathetic and sympathetic activity.  I am re-assured that I appear to be at low risk of a heart attack.


I suspect that the substantial HRV is the product of my training.  In future posts I will examine the evidence regarding the types of training that are most likely to improve HRV and also explore the question of whether measurement of HRV does in fact provide not only an estimate of likely risk of a heart attack, but also might be a useful indicator of the over-training syndrome, and hence provide a useful way to adjust one’s training schedule.

High intensity v low intensity training for the heart

June 23, 2009

My post on 20th 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 20th June) and high intensity interval training can produce benefits, but high intensity interval training is the more efficient.

Hypertrophy and the supply of blood to heart muscle

June 20, 2009

There are two main reasons why a runner might be concerned about the best way to train the heart. First, to improve running performance and second, to increases life expectancy or at least minimize the risk, albeit small, of heart attack during or after a race. As discussed in recent postings there are at least four aspects of heart structure and function that respond to training: blood supply, muscle hypertrophy, efficient fuel metabolism and heart rate variability (HRV). The relevance of HRV to perhaps less easy to appreciate, but as discussed in my post two days ago, decreased HRV appears to be a risk factor for sudden cardiac death.

In today’s post I want to examine cardiac muscle hypertrophy and improved blood supply. The reason for considering these two types of adaptation together is that the most important feature that distinguishes the healthy cardiac hypertrophy for the unhealthy hypertrophy that can occur in patients with cardiovascular disease, is the concurrent development of both muscle hypertrophy and blood vessels in healthy ‘athletes heart’, in contrast to hypertrophy without increased blood supply in pathological conditions. There is strong evidence for mutual interaction between the processes that promote normal development of muscle and blood vessels in the heart.

Back to the mini-pigs

Before examining the evidence from studies of human athletes, it is worth returning to the study of Yucatan mini-pigs which I mentioned a week ago. Pig heart has many similarities to human heart, but it is possible to do much more comprehensive investigations of changes in the pig heart. In that study by White and colleagues (J Appl Physiol 85:1160-1168, 1998) the pigs underwent an aerobic training program similar in volume and intensity to that typical of a long distance runner’s base-building program. The pigs were trained to run on a treadmill at a heart rate in the range 70-80% of maximum. In the first week they ran for 30 min on 5 days per week. The daily duration was increased by 5 min per day each week in the first 8 weeks and thereafter they continued to run for 70 min per day 5 days a week until 16 weeks.

During the first three weeks, the density of capillaries supplying blood to heart muscle increased, and then in the remaining weeks these capillaries apparently enlarged to become arterioles, so that by the end of 16 weeks, the cross sectional area of blood vessels had increased by 37%, and coronary blood flow had increased by 22%.

Capillary transfer reserve, which was assessed by measuring the increase in transport of diffusible molecules from blood to muscle when vessels were maximally dilated by administering a vasodilating drug, increased steadily throughout the study and at 16 weeks was 59% greater than at baseline. This demonstrates not that not only was the resting blood flow increased be training, but the capacity to increase the delivery of oxygen and nutrients to the heart under conditions of high demand was increased even more dramatically.

Left ventricular mass (relative to total body mass) had increased by 16% at 8 weeks and 24% at 16 weeks. VO2max increased by almost 40% in the first 8 weeks and thereafter only increased slightly. Thus a 16 week program of aerobic training produced an initial rapid development of new capillaries. Very little new sprouting of capillaries occurred after 3 weeks, but the total cross sectional area of blood vessels continued to increase, apparently reflecting the conversion of capillaries to arterioles, while muscle hypertrophy continued throughout.

Studies of humans

Many studies have revealed that athletes exhibit cardiac hypertrophy relative to sedentary controls, but there are remarkable few longitudinal studies that allow an estimate the magnitude of the effect of a particular training program on cardiac structure and function. Furthermore, it is necessary to consider the issue of the stage in an athletes career. One might expect the greatest gains in the early years, though of course this must be set against the expectation that training volume and intensity should be less in the early stages of a running career.

Moderate intensity training in novices

In a study by Rodriguez et al Am J Cardiol.;97:1089-92, 2006), 23 sedentary men in their late 20’s and early 30’s undertook a 6 month program of moderate-intensity aerobic training (1 hour/day, 3 times/week). This program achieved a 14.5% increase VO2 max; a 4 beat per minute decrease in average resting HR; a 15% increase in left ventricular mass index; and approximately a 6% increase in thickness of both the septum separating the ventricles and the posterior ventricular wall (assessed by Doppler echocardiography). Somewhat surprisingly there was not a statistically significant increase in stroke volume. Nonetheless, this study clearly demonstrates substantial left ventricular hypertrophy and also an associated increase in VO2 max during the type of 6 month aerobic program that might be recommended for novice who has recently taken up running.

Intense training in elite athletes

Perhaps of more relevance to committed athletes is a study of changes during the 6 months training commencing at the end of a 6 week off-season, in a cohort of 22 young elite athletes, by Naylor and colleagues from University of Western Australia (J Physiol 563; 957-963, 2005). The athletes (all rowers) had a mean age of 20, suggesting a prior career of 3-5 years duration. At the beginning of training after the off-season they had a mean left ventricular mass of 235 gm compared with 178 gm in a group of matched recreationally active control subjects. After three months training (twice daily, 6 or 7 days per week), the athletes had increased their left ventricular mass even further to 253 gm and it then remained stable around this level (with a value of 249 gm at 6 months). Thus it appears that there is a cumulative increase in hypertrophy over years of training, at least in young athletes, and training in the new season can produce a further increase around 7% in the first 3 months followed by a plateau period extending out to 6 months (ie a lesser relative increase than the 15% reported by Rodriguez in the 6 month program in novice subjects).

However the even more interesting measurement in the elite athletes studied by Naylor was left ventricular flow propagation velocity, an indicator of speed of left ventricular filling. At the beginning of the season, this quantity was less in the athletes than in the control subjects. Rapid filling is required to make the most of the benefits of greater contractility. It appears that a hypertrophic heart is of little value if it is not regularly exercised. However left ventricular filling rate improved throughout the 6 months of training, to a level marginally higher than that in the non-athlete control subjects. Thus by the end of the 6 month training period the athletes had hearts that were not only larger than the controls but also filled at least as rapidly.

It should be noted that the rowers studied by Naylor engaged in a mixed training program including both aerobic and resistance training. It was once believed that aerobic training produced predominantly an enlargement of the ventricular diameter, and hence stroke volume (so called eccentric hypertrophy), while resistance training produced thickening of the ventricular walls (concentric hypertrophy). More recent evidence indicates that enlarged diameter does predominate slightly in endurance-trained athletes whereas increased wall thickness predominates slightly in resistance- and static-trained athletes, but the differences are not dramatic (Barbier et al, Herz 31, 531-543, 2006).

Mechanical mechanism of hypertrophy

The mechanism of hypertrophy can be investigated at various levels. At the level of large scale mechanical processes it is well understood that increased filling of the chambers of the heart will stretch the vessel walls and this will lead to increased tension in the muscular walls which will in turn result a more powerful contraction (the Frank Starling Principle) – similar to the greater power of skeletal muscles during plyometric exercise. This greater stretching acts as a stimulus to hypertrophy.

Underlying molecular mechanisms

However perhaps more interesting is the mechanism at the level of the molecular processes that go on within the muscle cells. As is the case in many biological processes, effects occurring at the cell surface (eg mechanical effects such as stretching or the binding of messenger molecules) initiate a complex cascade of signaling within the cells. This intracellular signaling usually involves activation of enzymes that add phosphate groups to other proteins thereby changing their shape and function, and these proteins then act on others creating a cascade of effects. The signaling processes lead to the expression of genes (that is, the translation of the DNA code) to produce new proteins, which might themselves be either additional signaling molecules, or the proteins that carry out the primary function of the cell – e.g. contractile proteins.  Thus the  end result of the cascade of signals is the production of proteins that carry out the main functions of the cell. 

One of the pathways involved in cardiac muscle hypertrophy is the Akt pathway (Shiojima & Walsh, Genes Dev. 20: 3347-3365, 2006). Akt is activated by various extra-cellular stimuli. One of the mechanisms of activation is via insulin-like growth factor (IGF). A comparison of professional soccer players (who trained for 10 hours per week) with non-athletes, revealed that IGF formation is associated with cardiac hypertrophy (Neri Serneri et al, Circ. Res. 89;977-982, 2001). The authors concluded that increased cardiac IGF is likely to be a major contributor to cardiac hypertrophy in athletes. Akt is a signaling molecule that itself acts on three different pathways: pathways involving GSK-3, m-TOR, and FOXO. [The names of signaling molecules should be read in the same spirit as Jabberwocky, or perhaps, like the names of fundamental particles in physics – some names have an understandable serious origin but others sound like a private joke between the scientists who created them]. GSK-3 regulates cardiac muscle hypertrophy; m-TOR regulates growth of small blood vessels (possibly be the well known vascular endothelial growth factor, VEGF). Akt switches off FOXO, which plays a role in protein degradation.

A crucial feature is that transient bursts of Akt signaling promote concurrent development of both muscle fibres (hypertrophy) and also development of capillaries. Concurrent hypertrophy and increase in capillaries is the characteristic of healthy hypertrophy. However paradoxically sustained Akt activity can result in the hypertrophy without accompanying development of small blood vessels. This is the characteristic feature of pathological hypertrophy seen in several form of heart disease. Although I am not aware of any evidence that excessive training can lead to hypertrophy without increased blood supply to the heart muscle, the observation that sustained Akt activation can have potentially pathological effects points to the need for the body to have mechanisms that protect against excessive training. My own speculative hypothesis is that the over-training syndrome, which acts to discourage an athlete from continuing with an excessive training routine, might indeed be a defensive mechanism invoked by the body to protect us from ourselves. I will return to this theme in a later post.

Practical conclusions

So in conclusion, the main goals of a distance runner, namely improving blood supply to heart muscle and producing the hypertrophy associated with an increase in stroke volume, can be met simply an aerobic program along the lines undertaken by the Yucatan mini-pigs studied by White and Bloor. However, the study by Naylor of elite athletes in the six months following the off-season demonstrates the complexity of the relationship between prior training history and the improvement in cardiac function. In particular, the evidence indicates that despite the persistence of previously acquired hypertrophy, deterioration in ventricular filling speed during a 6 week off-season might offset any advantages of the pre-existing hypertrophy until many months after the resumption of vigorous training. There is not a great deal of evidence to demonstrate superiority of one training regimen over another for improving cardiac function, but nonetheless, I will review what evidence there is, in the near future.

Heart rate variability: is the debate between Noakes and Ekblom about the wrong question?

June 16, 2009

In my recent post about training the heart I listed three aspects of heart structure and function that respond to training: blood supply; muscle hypertrophy; and fuel metabolism. There is a fourth which is less easy to understand, but might actually be the most important. So bear with me.  We will get back the the reality of every-day training before too long.

The fourth trainable aspect is heart rate variability (HRV); the variability in heart rate that occurs on a time scale of 2 to 20 seconds. It is well established that the heart rate varies breath by breath, inceasing during inspiration and decreasing during expiration, mainly due to input from the parasympathetic nervous system during expiration. Furthermore it is established that loss of this heart rate variability is a predictor of risk of sudden cardiac death. Finally, many stressors, including hard training or racing cause a reduction in heart rate variability and the degree of this reduction is correlated with the length of time it takes for the body to recover.  It should be noted that many different types of stress, possibly involving signals from different systems within the body, can produce a reduction in HRV.  It appears that a healthy heart requires resilience

Back to the central governor

For the past decade Tim Noakes in Capetown (J Appl Physiol 106: 347, 2009 and 106:341, 2009.) and Bjorn Ekblom from the Karolinska Institute in Stockholm (J Appl Physiol 106:339-341, 2009) have debated the issue of the central governor – a proposed governor in the brain that acts to limit power output so as to protect the heart. The debate between Noakes and Ekblom centres on the fact that even at a power output around VO2 max, there is good evidence that under many circumstances there is substantial coronary reserve (ability to increase coronary blood flow) and also ability to increase cardiac work. Ekblom has invoked this evidence to oppose Noakes theory of the central governor [Ekblom, Scand J Med Sci Sports 2000: 10: 119–122; J Appl Physiol 2007; 102:781-786 ] As far as I can see, Ekblom has got the best of the argument, at least in the eyes of many professional physiologists, though many athletes are more sympathetic to Noakes.

In my view, both Ekblom and Noakes might be asking the wrong question. If indeed it is loss of heart rate variability rather than simple deprivation of oxygen that puts the heart at risk, an effective governor will be geared up to identify serious decrease in HRV and at that point, limit the body’s power output.

Why might HRV be the key?

This seems plausible for several reasons. First of all, most deaths during or after a marathon do not occur when the heart is likely to be acutely deprived of oxygen, but rather following cumulative stress (Journal of the American College of Cardiology, vol 28, pp 428-431, 1996).  Cumulative stress decreases HRV. Secondly, the fact that decrease of HRV predicts recovery time from a race or training suggests that the brain not only keeps track of HRV but sets this in the context of how much longer the race will be. This would explain the observation that it is possible to sprint at the end of a marathon even when it was impossible even to increase pace slightly after hitting the wall a few miles earlier.

Why is it hard to improve max HR by training ?

This proposal provides a simple answer to the question of why peak heart rate is virtually non-responsive to training and tends to decrease with age, thereby resulting in decreasing VO2max and decreasing aerobic performance. A rise in HR is associated with an increase in sympathetic input; a decrease in parasympathetic input; and a decrease in HRV. At a certain heart rate, it would be dangerous to decrease parasympathetic input any further. As the tissues of the heart become stiffer with age, this might be expected to occur at a lower HR. This raises the crucial issue of whether training can prevent this deterioration. I will return to that issue later.

Nerves supplying the heart

To propose that Noakes and Ekblom have been arguing about an irrelevant measurement is a rather a bold claim to make, so you might reasonably expect me to provide some better evidence. The first body of evidence concerns the nerve supply to the heart. There is an internal nerve supply in the heart (Arora et al , Am J Physiol Regul Integr Comp Physiol 285: R1212–R1223, 2003), and also an external input from the two main divisions of the autonomic nervous systems: the sympathetic system which makes the heart beat faster and the parasympathetic system that slows the heart down

Sympathetic input rises under stressful circumstances while parasympathetic input increases during relaxation or recovery. Sympathetic input to the heart causes slow oscillations in heart rate (on a time scale of 7-20 second2); parasympathetic input causes more rapid oscillations on a time scale of 2-7 seconds. There is a great deal of evidence that a preponderance of slower parasympathetic oscillations predicts a longer life. Spinal cord stimulation which is likely to send parasympathetic signals to the heart tends to overcome the dangerous effects of oxygen deprivation in a diseased heart, and can be an effective treatment for angina (Foreman et al Cardiovascular Research 47;367–3750: 2000).

The heart talks to the brain

Furthermore the passage of nerve messages between heart and brain is not one way. The nerves in the heart send messages back to the brain, providing a means of informing the brain about the current variability and stress level. However the internal cardiac nerves cannot by themselves produce the heart rate variability that appears to be a feature of health. In a dog with the sympathetic and parasympathetic input removed surgically, coordinated rapid contraction of the heart occurs but HRV is abolished (Murphy et al Am J Physiol Regulatory Integrative Comp Physiol 266:1127-1135, 1994). There is a large body of evidence indicating that HRV predicts the amount of extra oxygen that will be required after a hard training run – and this does not appear to be simply a matter of the brain estimating the accumulation of lactate, at least when the heart has been under substantial stress (Dixon, Cardiovasc Res. 26(7):713-9,2000).  Suunto, who manufacture a heart rate monitor that can measure HRV, claim that loss of HRV might be a useful indicator of over-training. I think the evidence regarding detection of over-training is complex, but there appears to be a degree of truth in Suunto’s claim.

What does this mean for planning a training program?

If some or all of these speculations are correct, the crucial issue for the athlete is whether HRV can be improved by training. The good news is yes (eg Dixon, Cardiovasc Res. 26(7):713-9, 1992). In the near future I will return to the discussion of how we can best train the heart, and at that point I hope to provide a good answer to this question.

Meanwhile, with regard to Ewen’s comment after my post on Saturday suggesting that he is limited by his muscles, not his heart, I agree, but I would propose that it might be that his current strenuous training and relativley unremitting program might have led to a reduction in HRV. Hence, his central governor is acting to stop him pushing himself too near to VO2max. Ewen, do you have a HRM that will provide you with HRV values? I apologize in advance if I am shooting off with an unfounded hypothesis.

Cardiac fitness

June 13, 2009

Recently I said that I would post some thoughts on running and the heart. The topic is vast. Today I want to address the question of whether athletic performance is limited by fitness of the heart or fitness of the skeletal muscles. This has been a topic of debate since the 1920’s when Nobel prize winner, AV Hill, first put forward the concept that a governor protects the heart by ‘slowing the circulation’ (Quart J Med 1923;16:135–71). In the past decade, two of the main protagonists in the debate have been Tim Noakes in Capetown and Bjorn Ekblom at the Karolinska Institute in Stockholm. As might be expected, the answer appears to depend on circumstances.

Can cardiac work increase at power output above VO2max?

Ekblom and colleagues (J Appl Physiol 2007; 102:781-786) measured oxygen utilization (VO2), cardiac output, heart rate and blood pressure in 8 well trained young men during two brief bouts of exercise (lasting about 4 minutes each) at a power output above that achievable at VO2 max. During these bouts of ‘supramaximal’ exercise (i.e. above power output at VO2 max), blood pressure rose with increasing power output despite constant VO2 and heart rate, demonstrating that the work done by the heart continued to increase. This suggests that the cardiac work under the circumstance of that study was not the limiting factor.

What happened to cardiac output when the oxygen supply is low?

In contrast, in a review of studies of cardiac output when running at high altitude (or other circumstances where a decreased amount of oxygen is delivered via the lungs) by Noakes’ team, suggests that under these circumstances, cardiac output falls as availability of oxygen falls (Journal of Experimental Biology 2001; 204, 3225–3234). If the heart was not the limiting factor, it might be expected that cardiac output would rise to maintain the rate of delivery of oxygen to skeletal muscles. However, this might be a risky strategy. Increasing cardiac output and therefore increasing the oxygen requirements of the heart, when the availability of oxygen is less would create the risk of starving the heart muscle of oxygen, thereby creating the risk of disturbance of the exquisitely synchronized rhythm of heart muscle contraction and potentially fatal fibrillation. Perhaps not surprisingly under conditions where oxygen delivery via the lungs is less (eg at high altitude), it appears that Noakes ‘central governor’ takes action to prevent the heart being damaged with catastrophic consequences.

My central governor

My asthma frequently restricts the supply of oxygen to my lungs. I do not regularly measure my peak expiratory flow before and after training, but when I do, it typically falls from around 500 litres per minutes to around 250 litres/minute during a training session. The most extreme I have observed was a fall from 610 litres per minute to 130 litres per minute. My subjective experience is that over shorter distances, I am limited mainly by my ability to get enough oxygen into my lungs. Interestingly, I find it very hard to get my heart rate much above 150 (though on some occasions I do manage to get it to 160). I suspect that my non-conscious brain is very reluctant to allow me to push myself to the limit. So the effect of diminished oxygen supply is not a compensatory increase in heart rate, but rather my brain appears to curtail how fast I can run, possibly to protect my heart.

In fact I have little desire to push myself to VO2 max and beyond at present. I would quite like to run a fairly fast mile again one day (ie, anything faster than 6 minutes – the pace that I once regarded as the slowest worthwhile training pace even for long distance runs, but at present I am unable to sustain that pace for even one mile), though I am prepared to put that day off until my asthma settles. I use a steroid inhaler which keeps my asthma under moderately good control. So far I have resisted taking oral steroids; I would only accept the risks of oral steroids if asthma was seriously interfering with my everyday life. For the time being I would prefer to work on gradually building my aerobic capacity and increasing the endurance of my leg muscles, since those are the characteristics that limit me when running long distances in the aerobic zone. Nonetheless, I am also eager to increase my cardiac fitness as much as possible to give myself a good buffer zone so that I can safely push myself a little beyond lactate threshold at the end of a race.

Creating a safety buffer zone

Cardiac deaths among athletes are not restricted to those competing in short anaerobic events. The risk of cardiac death in the 24 hours after a marathon is estimated to be around 1 in 50,000 (Journal of the American College of Cardiology, 1996; 28, 428-431). This is a small risk but nonetheless, even among those who do not suffer asthma or any known cardiac disease, it would seem to be worthwhile to increase cardiac fitness as much a possible before strenuous endurance events. But this raises the question of how can we best make the heart fitter?

First we must ask what aspects of heart structure or function can be strengthened by training. There is good evidence that training can produce improvements in three main domains:

1) Hypertrophy of cardiac muscle. Both ventricular diameter (and hence stroke volume) and also cardiac wall thickness can be increased by training. When I was young, there was much discussion as to whether or not the hypertrophy of an athlete’s heart was healthy. In non-athletes, a large heart can be a sign of serious disease. In the past few decades it has become clear that the hypertrophy seen in athletes is generally healthy. Unlike pathological hypertrophy, which is usually associated with decreased coronary reserve ( decreased ability to increase blood flow in the coronary arteries when required), in athletes cardiac hypertrophy is usually associated with increased coronary reserve (Hildick Smith and colleagues, Heart 2000;84:383–389).

2) Increased capacity of small blood vessels supplying the heart muscle.  The evidence for this was controversial for some years because some measurements suggested that capillary density was not increased in athletes compared with sedentary people. However, this debate was resolved by a study of Yucatan mini-pigs carried out by White, Bloor and colleagues (J Appl Physiol 85:1160-1168, 1998.) Pig heart resembles human heart in many ways. White and colleagues trained their pigs on a treadmill for 16 weeks, following a program that entailed a gradual increase from running for 30 minutes, five days per week at 70-80% maximum heart rate, up to running for 70 minutes, 5 days per week, after 8 weeks. The pigs maintained that training load for a further 8 weeks. After the initial 3 weeks capillary density had increased, but at 16 weeks capillary density was not greater than at baseline – however the number of arterioles (blood vessels intermediate in diameter between capillaries and arteries) was increased, indicating that number of capillaries had initially increased, but subsequently the diameter of these capillaries increased and they became arterioles.

The most important aspect of coronary blood supply for the athlete is how much it can increase above resting level when required. This is known as coronary reserve. It is probable that coronary reserve depends not only on the number and diameter of blood vessels, but also on the hormonal or other biochemical mechanisms that produce dilation the blood vessels when demand increases. Another similar measure that is more appropriate for measurement in animals, is capillary transport reserve. In White’s study of Yucatan mini-pigs, capillary transport reserve increased even more dramatically than coronary blood flow. Whereas blood flow increased by 22%, capillary transport reserve increased by almost 60%

3) Increased capacity for metabolizing fuel to produce energy. One of the metabolic adaptations that occurs with training is an increase in the ability to transport lactate from the blood stream into the heart. In general heart muscle works in the aerobic zone, but it can nonetheless use lactate (produced for example by skeletal muscle) as fuel. The transport system that moves lactate across the sarcolemma (cell membrane) of heart muscle responds well to training (Bonen, Eur J Appl Physiol, 2001, 86, 6-11) It seems to me that this might be a very valuable adaptation for the long distance runner. If blood glucose reserves begin to fall in the later stages of a long run in the upper aerobic zone, the capacity to utilize the lactate that has accumulated in the blood following extrusion from skeletal muscle, should at least ensure that the heart has an adequate supply of fuel.

White and Bloor’ study of Yucatan mini-pigs demonstrated that a training program similar to that which might be recommended for base building prior to a half marathon or marathon program (though perhaps a little monotonous for my own taste) resulted not only in increased small blood vessels number and diameter, but also increased capillary transport reserve and cardiac muscle hypertrophy. However, not all types of training produce the same profile of benefits for the heart. In a future post, I will examine what little evidence there is regarding the optimum training program for achieving improvements in each of the different aspects of cardiac fitness.

Furman re-visited

June 7, 2009

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 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 4th 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 5x1Km 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.


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 31st.  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.