I have been pre-occupied with fatigue in recent weeks, but I think that is now behind me.  For me, the most interesting thing as been the fairly clear evidence from my heart rate recordings that my non-conscious brain imposed a limit (mediated by the parasympathetic nervous system) on how much work my heart was able to do.   While I think that limit was initially based on a non-conscious but sensible protection strategy, it eventually because over-protective.   Furthermore, I think it is likely that my conscious strategy of graded exercise to teach the non-conscious part of my brain that regulates the autonomic nervous system, that it was safe to relax the limit, allowed me to recover fairly rapidly.

Ironically the final test of my recovery strategy was at the price of thrashing my legs beyond their current ability to cope in the Robin Hood half marathon.  So I am now nursing strained hip adductors.  However they are recovering. The bruising that tracked down the medial aspect of my thigh from near the point where adductor longus attaches to the femur has now turned yellowish-purple. In the past two days I have done very gentle runs of around 6Km without any sign of fresh bruising.  However it has been noteworthy that my legs are still tired, confirming that the adductor strain was merely a crunch that might have easily struck in any of the other major leg muscles.  In some ways I am pleased it was the adductors because shortening my stride allowed me to continue with relatively little further damage.  Maybe a tear of the hamstrings or quads would have stopped me from doing any further damage, but on balance, I am really pleased that I was able to finish.    For the next week or so, it will be gentle exercise to promote recovery while trying to avoid tearing the healing fibres apart.

Fatigue is a complex thing

While it appears that the parasympathetic action of the heart was the mechanism of my recent fatigue, I suspect that many instances of the more transient fatigue that sets in during long races are mediated by other mechanisms, especially by mechanisms that act directly on the leg muscles. 

One of the great things about the blogs by amateur runners is the insight they provide into what goes on in the mind and body during a long race.  I am cautious about expressing my thoughts about other people’s blogs in my own blog, but overall, I consider that what people have freely put into the public domain is legitimate material for comment.  I am therefore inclined to put down my speculations about the report on the Dingle marathon a week ago, by Thomas (Diary of a Rubbish Marathon Runner, http://rubbishrunner.blogspot.com/) though I should start with the caveat that my speculations  say more about me than about Thomas.  Nonetheless I will let Thomas know that I have written about him so he can correct any mis-perceptions on my part.

Thomas’ experience is especially informative because he is one of the most determined and motivated of those runners whose blogs I follow. Therefore I think it can be taken for granted that a far as conscious determination goes, few runners would approach a race with more dedication and determination than Thomas approached the Dingle marathon.  As the event unfolded, I think he ran an excellent race; his time and placing are, beyond doubt, great achievements.  He did not achieve a personal best, and one does not need to look far for the obvious explanations: an unseasonably warm day, and a brutal hill in the final few Km of the race. 

However, if one approaches the evidence with a mental bent towards understanding how it was that these two circumstances influenced Thomas’ race, several more intriguing thoughts arise.  

Background

But first we need to look at the background.  Thomas achieved 3:05:37 in the Dublin marathon last year and has trained very hard and very effectively since then.  He ran a creditable 3:10:36 in Boston under difficult conditions in April this year.  As he approached Dingle, his training paces demonstrated that he had the potential for a sub- 3 hour marathon under favorable circumstances.

At Dingle, circumstances were not favorable.  After miserable weather through July and August, Saturday 12^th September proved to be one of the most glorious days of summer for anyone except a marathon runner.  The temperature in Dingle was 22 degrees C (72 degrees Fahrenheit). 

Acclimatization to warm weather

There is no doubt that humans acclimatize to warm weather, though having spent my childhood in Adelaide, South Australia, I have often wondered about the mechanism of acclimatization.  Adelaide has cool winters and warm summers.  In early spring, when the temperatures first exceed 75 degrees Fahrenheit (we used the old units in those days) it felt great, but almost too hot for comfort.  A few months later,  we considered that we were being cheated of our summer if the temperature was not regularly in the upper 80’s or low 90’s,  and as children, we even took a perverse delight in times when the daily maximum temperature exceeded 100 degrees for several days on end.  I often trained in temperature well above 90 degrees and thought nothing of running a 5000m race on a mid-summer afternoon.

What had changed between the first days of spring and mid-summer only three months later?   There might have been changes in the function of our kidneys or sweat glands, but I suspect that the main change had been a change in what our brains accepted as normal. 

Jim Peters and Il Topolino

So what happens when we race on hot days?  Probably the winner of a long race on a hot day is the runner who is best acclimatized, but what does acclimatization entail?  Jim Peters’ collapse only yards from the line in the Vancouver marathon in 1954, while miles ahead of his rivals, suggests that the reason he was so far ahead was not due to a greater ability of his body to withstand heat, but rather an ability to over-ride his brain’s attempts to keep his body temperature within safe limits.

Don Thompson’s gold medal in the 50K walk in Rome in 1960 provides another thought provoking illustration.  Thompson, who was nick-named Il Topolino (‘mighty mouse’) by the Italian crowds, was diminutive in stature but mighty in his spirit.  He had trained for Rome in an improvised hothouse in the bathroom of his mother’s house in Middlesex.  He installed a stove in the room and put on a kettle to boil; closed the door and window; and switched on the electric wall heater to augment the effect of the steaming kettle.  Years later, when asked how Paula Radcliffe should prepare for the marathon in Athens in 2004 his reply was: ‘I trained in the bathroom about three times a week, from May to September, but I didn’t stay in there long each time and I think it was more about a boost to my confidence.’  Maybe Il Topolino had trained his brain to believe that keeping up the pace when the temperature was above 80 degrees F was possible, rather than adjusting the function of his kidneys or sweat glands.

The scientific evidence

Scientific studies confirm athletes tend respond to hot weather by slowing down to minimize the rise in core temperature; rather than by slowing down once core temperature has already risen.  In a comparison of African and Caucasian runners during self-paced 8K treadmill runs performed under cool and warm conditions, Marino and colleagues found that both groups ran at similar pace in the cool conditions.  The Caucasians ran more slowly under warm conditions, but sweated more profusely and maintained similar body temperature.  Marino concluded that the observation that the African runners ran faster only in the heat despite similar thermoregulatory responses to those of the Caucasian runners suggests that the larger Caucasians reduced their running speed to ensure an optimal rate of heat storage without developing dangerous hyperthermia (Marino et al., J Appl Physiol, 96: 124-130, 2004).

The diminutive Il Topolino demonstrated in Rome that it is possible to train the brain to over-ride this mechanism, but the case of Jim Peters in Vancouver perhaps illustrates that it can be difficult to get the balance right.  Fortunately, Peters recovered quite rapidly after re-hydration.

Back to Dingle

So what happened to Thomas at Dingle?  The temperature was warm by Irish standards, but in fact not really all that hot, at least by Australian standards. However, Thomas had been training in cold and windy weather around the shore of Caragh Lake in Kerry.  To both his conscious and non-conscious brain it seemed hot.  Nonetheless, he started with a first mile of 6:51, almost exactly in line with his 3 hour target pace and he reports that first few miles went very, very well. He was running  easily, feeling relaxed and happy.  For much of the first half, the race continued to go very well.  He was holding a pace of around  7:05 pace per mile which would have given him a finishing time near to his PB of 3:05:37.  However, it is of interest to note from the traces he presents in his blog that has pace tended to slow slightly throughout the first half, and his heart rate to fall very slightly from a mean around 168 bpm between miles 1 and 3 to a mean around 166 bpm from miles 10 to 13, despite greater undulations in the course after 6 miles.   Was his brain, either consciously or unconsciously, protecting him from undue exertion?   He reported that at 10 miles he started to feel some signs of fatigue.  Nonetheless he was still running well until mile 19, when the pace record shows he ‘lost it.’ He slowed from a pace of 7:10 per mile around mile 18 to slower than 7:30 per mile around mile 20.  The undulations in the road make the precise figure irrelevant but there was a definite trend towards slowing despite a net fall in altitude of approximately 50 feet between mile 18 and mile 21. 

Something else was looming on the horizon.  He reports that as he approached the drinks station at mile 21 he ‘could see the mountain looming ahead. It reminded me very much of Connemara’s “Hell off the West”, and I was in no illusion about the task ahead. This was going to be tough’    Starting in the 22^nd mile the road ascended 300 feet, at times with an incline of 13%.  He struggled gamely to the top, but shortly after the summit he was pole-axed by cramp.  His blog provides a graphic description of the pain in his calf muscles.  After a few protracted and excruciating moments he managed to apply a counter-tension that relieved the cramp, and he finished with an exultant wave to the crowd in 12^th place in a time of  3:12:44.   

It was a great performance, and I think it is unlikely that Thomas could have done any better on the day.  It is probable that some physiological process such as electrolyte imbalance was the coup that pole-axed him on the final hill, but his prospects of a PB were gone by 21 miles.  At that stage his heart rate had already fallen below 165.  We do not know how much his body temperature had risen, but Marino’s study suggests it unlikely that it had risen to dangerous levels.  More likely, his brain was protecting him from the heat and from the mountain ahead.  Some non-conscious part of that brain was probably also aware of his electrolyte status, and integrated this information with the message from his conscious brain that things were about to get very tough.  

While it is unlikely that there was anything Thomas could have done to have overcome the sensible response of his non-conscious brain at that time, no matter how determined he was, I suspect that if he had trained in an improvised hot-house, as Il Topolino had done almost 50 years previously, his brain might have allowed him to sustain a faster pace between 3 and 21 miles.  But whatever the physiological limit proved to be – electrolyte disturbance, core temperature or something else, it is probably just as well that his brain did not allow him to run himself to a state of exhaustion in Dingle.  That wasn’t the right day or place for a PB.  His more recent blogs indicate that he is recovering rapidly, and after a two week recovery phase, he is about to begin his preparation for the Dublin Marathon in 5 weeks time.  I think there is a very good chance he will record a PB in Dublin, and if the weather is good, his goal of a sub-3 hour marathon is within reach.

I appear to have recovered from the fatigue that had hamstrung me in mid August. In recent weeks I have described the way in which my return to training following the episode of illness in June and July was thwarted by a peculiar inability to raise my heart rate during exercise.  I found it very difficult to maintain a pace faster than around 6 min/Km. The most dramatic illustration of the problem occurred in the final stages of a staircase session on the elliptical cross –trainer, when I found it crushingly difficult to maintain an output of 240 watts for 4 minutes.  When I subsequently examined the record of my heart rate, I discovered that it had reached 143 bpm at the 200 watt step on the staircase, and had not risen at all when I increased the power output to 240 watts, resulting in the need to generate the additional power via anaerobic metabolism.  The Poincare plot of R-R intervals between successive heart beats demonstrated extensive spread of the points across the 45 degree line, confirming excessive parasympathetic output.  My parasympathetic nervous system was clamping my output in an apparently over-vigilant attempt to protect my heart from doing too much work 

The morning orthostatic tests corroborated the evidence of parasympathetic excess.  The rise in heart rate from resting to standing was typically only 2 or 3 beats per minute, compared with my more usual heart rate rise of around 9-10 BPM.  On one occasion, on the day following a very sluggish 16 KM run, my hear rate was actually lower while standing than when lying down, providing an additional illustration of an excessive parasympathetic response. 

 Today

Today, the pattern was much different. Here is a chart showing my heart rate during the orthostatic test, and also the Poincare plots representing R-R intervals in the 3 minutes before standing and during a 3 minute interval starting 30 seconds after standing (once the immediate heart rate variations associated with the work done in elevating by body had settled). 

Orthostatic test on 12th September 2009. The upper figure is the trace of heart rate while resting for 3.5 minutes and after standing for a similar period. The lower figures are Poincare plots of heart beat R-R intervals during the final three minutes of rest (left) and during a three minute period starting 30 sec after standing (right).

The features of note are:

1)      The orthostatic increase in heart rate is 14 bpm – a little greater than my normal increase of 9-10 bpm and much greater than the -1 to 3 bpm characteristic of the period when I was fatigued.

2)      There is much greater variability of heart rate while resting than while standing.

3)      While both resting and standing, the heart rate shows prominent fluctuation in time with my breathing.  I tend to breath naturally at a rate of around 6 to 7 breaths per minute when relaxing, a rate that corresponds to the 6 to 7 peaks per minute (0.1 – 0.12 Hz) in the heart rate trace.

4)      While resting, the breath by breath fluctuations exhibit a steady rise followed by a sharp descent.  I was aware of breathing out immediately prior to standing, a period in which the heart rate trace shows a sharp descent, confirming that the sharp descents arise as a result of the increase in parasympathetic output during expiration. These sharp descents are much less pronounced during standing.

5)      Comparison of the Poincare plots reveals not only a much greater variation in R-R intervals during rest (note the different scales marked on the axes) but also a different shape.  During the resting period, there is a cluster of points located far above the 45 degree line to the left side of the chart.  These points represent long intervals (ie slow heart beats) immediately following shorter intervals (faster beats), and reflect the sharp descents during expiration seen in the heart rate trace.   In contrast, the Poincare plot during standing is shaped like a comet with a flared tail.  It shows limited spread across the 45 degree line and relatively greater spread along the 45 degree line (though the actual extent is substantially less in both directions compared to the resting period).

Overall, today’s orthostatic test confirms that my parasympathetic nervous system is no longer over-active.  If anything, the balance has tipped further towards sympathetic activity compared with my usual state, though this degree of sympathetic output is well within the normal range.

 What led to recovery?

I am inclined to attribute my recovery over a period of 2-3 weeks to my program of low-volume, moderate intensity running.  I have done 3-5 runs per week, over distances of 3-6Km, either at an easy pace interspersed with a few moderate intensity stride-outs for a distance of 200-300 metres, or moderate intensity tempo runs. In addition I have done 1 or 2 staircase sessions on the elliptical cross trainer spanning the aerobic range (though on the one occasion noted previously, following an ill-advised attempt at a longer run the previous day, I found myself in the anaerobic zone at the top of the staircase, due to my parasympathetic system clamping my cardiac output).

 A decision about the Robin Hood half marathon

I am now ready to resume normal training.  This presents me with the need for a decision.  Tomorrow is the day of the Robin Hood half-marathon, which I had set as a target race four months ago.  The fact that I have not been able to train normally for the past twelve weeks has torpedoed any prospect of a fast time, and in any case, I would be unwise to push myself really hard on the first day back into normal training.

I am uncertain about what pace to set.  The greatest uncertainty is about how well my legs will cope with 21.1 Km, due to the marked truncation of training volume.  Here is a chart of my training volume in the period May to September this year, compared with the same period last year, when I ran the half-marathon in 101:50. 

Training volme (Km per week, averaged over 5 week intervals), May to September 2008 and 2009.

My training volume was greater last year, but most of that running was at low intensity.  This year, a higher proportion of the training sessions have included at least some moderate intensity running, and as a consequence, I think my aerobic capacity is probably not much less than last year despite my illness and its aftermath.   In several of my runs in the past two weeks, my heart rate has been around 650 beats per Km – over distances of 2-4 Km.  Last year, I rarely achieved lower rates than 650 beats/Km, though my endurance was much greater.

Although it is usually not sensible to set race pace according the heart rate on account of the risk of being misled by the higher sympathetic output associated with racing, in my present circumstances it is crucial that I avoid stressing my heart too much, to avoid precipitating another parasympathetic clampdown or perhaps an even more serious rhythm disturbance.  Hence, I think that the best strategy is to aim for a heart rate in the range 134-137 (upper part of the mid-aerobic zone) for the first 14 Km, and then adjust my pace according to how well I am coping at that stage.

The goal and the strategy

The evidence suggests that my strategy to overcome my recent acute fatigue syndrome with short sessions that include some moderate intensity running might be working.  The goal is to re-train my brain to accept that my body can safely cope with producing at least a moderate power output.  In my post last Monday (31^st Aug), I compared the Poincare plot of heart inter-beat intervals recorded during an elliptical staircase session during a mild setback on my path to recovery, with a plot from a similar session in mid-July before the onset of fatigue.  The feature of interest was the extensive spread of points across the 45 degree line on 31^st August, indicating excessive input from the parasympathetic nervous system.  This was apparently responsible for the fact that my heart rate could not rise above 143 bpm (averaged over 5 sec intervals), when I increased my power output from 200 to 240 watts.  I had to rely on anaerobic metabolism to generate the increase in power.  This was extremely demanding and in retrospect it was not surprising I found it very difficult to maintain 240 watts for more than a few minutes.  Clearly if I want to be able to produce a moderate power output, it was necessary to teach my non-conscious brain that it could relax the tight control at least a little.

Executing the strategy

During the past week I have done three elliptical sessions and two runs, each relatively short but each including a small amount of moderate intensity activity.  The increase in my heart rate from resting to standing during the orthostatic tests in the mornings has stabilized around 5 bpm – still a rather small increase, but probably within my normal range.  Encouraged by the signs of recovery, I repeated an elliptical staircase session on Friday.  To avoid the risk of stressing my heart too much, I spent only 2 minutes at each level of power output in contrast to 4 minutes at each level on previous occasions.  When I increased my power-out to 240 watts, my pulse rose to 147 bpm.  Although producing this power output required some effort, it was not so crushingly difficult as it had been when my maximum heart rate had been clamped at 143 bpm by my tyrannical parasympathetic nervous system, on 31^st August. 

Here are the Poincare plots for the three elliptical staircase sessions: mid-July, 31^st  August and Friday (4^th September).  The plot for Friday’s session is not fully comparable with the other two, because it was recorded after only 27 minutes of exercise, compared with 52 minutes in the other two sessions, and furthermore, the plot is based on a sample of heart beats over 1 minute rather than 2 minutes (because the plots can be misleading during a period of increasing heart rate immediately after an increase in power output).  Nonetheless, the three plots are as comparable as can be achieved in the circumstances.  The crucial point of interest is that the spread of points at right angles to the 45 degree line, which represents parasympathetic activity, is back to a level similar to that in mid-July.  This amount of spread is represented by the quantity, SD1, which was 4 ms  in mid-July; 13.4 ms on 31st August and 3.1 ms on 4^th September.   This provides further confirmation that the over-zealous parasympathetic nervous system that had clamped my cardiac output on 31^st Aug, forcing me to employ anaerobic metabolism to produce even a moderate power output, had learned by yesterday that it could safely allow the rise in heart rate necessary to generate 240 watts aerobically.         

Poincare plots of interbeat intervals in the upper aerobic zone during elliptical sessions before the onset of fatigue (July); during fatigue (August); and during recovery (September)

It is of course ironic that I am celebrating being able to push my heart rate to 147 in order to achieve a power output of 240 watts.  In June, I was pleased when I managed to produce 240 watts at a heart rate of 141.  However, in June my heart rate increased steadily as power output increased.  As I increased output from 200 to 240 watts, heart rate rose from 132 bpm to 141 bpm – in other words, in June, my relatively low heart rate was not due to clamping by the parasympathetic nervous system, but simply the result of being fitter.  ( It is not surprising that my aerobic fitness has decreased somewhat since early June, due to my illness and the fatigue that developed in its aftermath.  The increase in heart rate at 240 watts from 141 bpm in June to 147 bpm yesterday appears to reflect a decrease of around 4% in my aerobic capacity.  That is not too bad in light of the severity of my illness in June/July.)

A short tempo run

Encouraged by the apparent success of my strategy of short, moderately intense training sessions, yesterday (Saturday) I decided to do a 4Km tempo run.  In my only previous running session this week, I had done an easy 5Km including 4 stride-outs of 200-300m at a pace of around 4:45 /Km.  At the time, it would have required great effort to have increased to a pace any faster than this.  Nonetheless, because of my growing confidence, yesterday I decided to aim for a pace of 4:40 /Km for the 4Km run.

After warming up, I set off running comfortably with a gentle breeze behind me and reached the half-way point in 9:18 (4:39 min/Km) with an average heart rate of 138 bpm.  I anticipated that when I turned into the wind, it would no longer feel like a gentle breeze.  As expected, I had to increase the effort and my heart rate rose rapidly to 145, but I felt fine.  I covered the return journey in 9:20 despite the head-wind, giving a total of 18:38 (4:39.5 /Km).   I arrived home very pleased with my progress.

 The next day

However, the crucial question is whether or not today’s orthostatic test would show any evidence of a parasympathetic clampdown indicating over-exertion yesterday.  In fact, this morning the orthostatic difference was 5.4 bpm which is virtually identical to the average value of 5.3 bpm for the entire week. 

Thus, at this stage it appears that I am recovering from the excessive parasympathetic activity that had apparently produced the feelings of severe fatigue I had suffered two weeks ago.  Overall the evidence of the past few weeks is consistent with my previous suspicion that my parasympathetic nervous system tends to be over-active.  Furthermore, the evidence of the past week supports the hypothesis that the non-conscious part of the brain that regulates the parasympathetic system can be trained to relax the tightness of its  grip on the control of heart rate.  The question of whether or not I could have achieved the same outcome simply by resting remains unanswered, though the evidence from clinical studies that graded exercise can promote recovery from fatigue inclines me to think that the low volume, moderate intensity program was the right thing to do.

Caution

I remain aware that the parasympathetic nervous system serves a crucial protective role and therefore, I must be cautious in trying to modify it.  It is likely that the parasympathetic clampdown and the associated fatigue arose because I had been a little too vigorous in the attempts in early August to regain fitness after my illness in June and July.  Therefore, I will continue carefully, but I am cautiously optimistic.

After a few weeks of debilitating illness in June and July I wasn’t sure whether or not to stick to my plan of running the Robin Hood half-marathon in September.  When I started running again in late July I began with easy or moderate paced runs of around 5-6Km,  it became clear that I had lost a lot of fitness, but I was enjoying running.   Then at the beginning of August I decided to put matters to the test and ran 15Km, starting slowly but increasing the pace gradually.  I was pleased to find that I felt comfortable at a pace around 5 min/Km in the second half of the run.  That settled the question. I would run the half-marathon.  I was uncertain about the target time to set myself, but provisionally set a target time of 100 min – only one minute slower than the target I had set several months earlier.

As for training strategy, my first objective was to try to re-establish a reasonable level of endurance; so I planned to build up the distance with fairly easy paced running, up to around 60 Km per week. By mid-August, things were going according to plan.   I had three runs of 16-20Km behind me, and several ‘tempo’ runs – though at that stage, tempo pace was not much faster than 5 min/km.  I planned do two easy-paced longish runs in the third week of August followed by a few upper aerobic runs to confirm my choice of target race pace. Then something peculiar happened.

Malign alien force or guardian angel?

On the third Monday of the month, I set out on the first of the two planned easy-paced longish runs.  For about 5Km, things went well.  I felt very relaxed running at a pace of 5:45 min/Km with a heart rate in the lower aerobic zone (around 122).  And then quite unexpectedly, all the energy drained away from me.  I struggled to maintain a pace of 6:30 min per Km.  My heart rate dropped to around 115 and my legs felt very heavy.  It appeared that I was battling some alien force.  For the next few Km I made efforts to push the pace but then realized that it was a pointless struggle.  It was clear that I was losing the battle against the alien influence.  However, apart from the lethargy and heavy legs I was not experiencing any physical symptoms.  My pulse was regular and strong, though reluctant to increase much above 115 bpm.  So I kept on plodding along wondering what it all meant.   In the end I covered 16 Km, but at times my pace dropped to 8 min/Km.

The next day I did a short easy jog and felt OK, so on the Wednesday I again attempted the planned long easy paced run, though on this occasion, aiming only for a pace around 6 min/Km.  I felt sluggish though at least I was able to get my heart rate above 120.   Again I managed to do16 Km, but it appeared that I was in no shape to race a half-marathon within a few weeks.  I took it easy, doing only short easy runs for the rest of the week, and on the following Monday made yet another attempt at a longish run.  Yet a third time, the alien force was holding me back.  I eventually settled in for a slow plod at a pace in the range 6:30 to 6:45 min per Km and heart rate around 110.

What was going on?  I had been experimenting with various fitness measures using my new Polar RS80CX heart rate monitor, and after some experimenting, I have decided that the orthostatic test appears to be the most practical and useful test for monitoring my response to training.  What is clear is that during that third week of August I was experiencing an excessive parasympathetic drive that was keeping my heart rate down.   Maybe I am not struggling against an alien force; more likely it is a tyrannical guardian angel that is trying to protect me from myself.

The orthostatic test

In the orthostatic test, heart rate is recorded lying down for three minutes and then standing for a similar period.  Heart rate increases after standing, to elevate blood pressure sufficiently to combat pooling of blood in the lower extremities and thereby ensuring adequate perfusion of the brain.  This increase in heart rate is achieved by a shift in the balance between the activity of sympathetic nervous system  (the adrenaline-based fight or flight system) and the parasympathetic nervous system (which generally promotes relaxation and recovery).   On standing, sympathetic activity increases and in a fit person, an increase in heart rate of around 10 bpm can be expected (McGee and Abernethy, Journal of the American Medical Association. 1999;281:1022–1029.).  In an unfit or stressed person, the increase is usually greater.  

However, sometimes there is a paradoxical surge of parasympathetic activity – blood pressure falls and the person collapses in a faint.  Recovery usually follows quickly provided the person remains lying down.  This paradoxical surge of parasympathetic activity – a so-called vasovagal attack- appears to reflect an over-active compensation mechanism that exists to prevent us from over exerting ourselves.

While a faint is transient and harmless, it is interesting to speculate on the similarities between a transient vasovagal event and two enigmatic conditions that are very relevant to athletes: fatigue and over-training.   But first it is relevant to examine the results of a study of orthostatic test responses in marathon runners

Orthostatic responses after a marathon

Gratze and colleagues carried out an orthostatic test on 51 healthy amateur marathon runners the day before the Graz (Austria) marathon in 2007 and 2 hours after completion of the event (European Heart Journal vol 29, pp 1531–1541, 2008).  None of the runners exhibited a vaso-vagal attack on the day before the race, but 14 did so on testing after the event.  These runners were classified as orthostatic intolerant.  As expected, all runners exhibited evidence of increased sympathetic activity (indicative of stress) after the event, but the 14 who were orthostatic intolerant were unable to generate the required increase in sympathetic activity to compensate for pooling of blood in the lower extremities during the test.  Instead they demonstrated a paroxysmal increase  in parasympathetic activity, and developed signs of incipient collapse.

The only significant predictor of risk of orthostatic intolerance identified by Gratze and colleagues was having serum potassium levels in the lower part of the normal range before the race.  However there was also a trend towards a higher training volume in the preceding 4 weeks in the orthostatic intolerant group. (The probability that the difference between groups would have been as large as that observed purely by chance was 6.9%.  Thus the possibility of chance cannot be ignored, but weighing up all the evidence makes me think that the difference is unlikely to be due to chance).  The orthostatic intolerant group also had a higher training volume in their lightest week in the preceding month – in other words, they had not tapered to the same extent as those who did not develop orthostatic intolerance.  This invites the speculation that the runners who developed orthostatic intolerance were on the verge of over-training.

Over-training

Improving fitness necessarily demands over-reaching – the transient deterioration in performance following hard training that stimulates the development of increased fitness during the subsequent recovery phase.  If the athlete does not allow time for recovery following a hard training session, over-reaching develops into the early ‘sympathetic’ phase of the over-training syndrome, characterized by over-activity of the sympathetic nervous system – the adrenaline-related component of the autonomic nervous system that generates the fight or flight response.   Provided this sympathetic phase of the over-training syndrome is recognized in time, reduction in training volume or intensity for a few days is usually enough to promote recovery. 

However, if it is not recognized, non-conscious neural mechanisms intervene to protect us from our own fool-hardiness.   Perhaps this guardian angel within our non-conscious mind might be described as the central governor – though this is not quite the context which led Tim Noakes to develop the central governor hypothesis.  Whatever the true nature of our guardian, he/she is scarcely an angel and the consequences of his/her intervention are not quite what we might wish – the parasympathetic nervous system which normally promotes healthy relaxation and recovery becomes a tyrant. 

The balance between parasympathetic and sympathetic activity tilts strongly towards parasympathetic excess.  We no longer have any drive for fight or flight .   We become listless, apathetic and find that getting the heart rate up into the upper aerobic zone demands a major effort. The body is unable to mount an adequate defence against either injury or illness, and eventually either injury or illness forces a cessation of training.  This is the parasympathetic phase of the overtraining syndrome, and can last for weeks, months or even years.  If the 14 individuals from the sample of 51 marathon runners studied by Gratze were indeed on the verge of the parasympathetic phase of the over-training syndrome, then the risk of this problem is not uncommon.

Wrestling with an over-protective nanny

One of the reasons I have become especially interested in the over-training syndrome in recent times is the fact that despite life-long mild asthma which had caused me no problems since infancy, I have been increasingly hampered by broncho-constriction, the defining characteristic of asthma, in the past two years.  I have also been aware of having a rather low heart rate suggesting a tendency towards parasympathetic dominance.  Broncho-constriction can be precipitated by parasympathetic over-activity.   The sympathetic ‘fight or flight’ response opens the airways, while the parasympathetic ‘rest and recovery’ system has the opposite effect.

When I read Hadd’s well known account of his client Joe, who was training for a 2:20 marathon, I was intrigued to note for the first few levels of the Hadd test (a series of 2.4 Km runs at incrementally increasing heart rate) that I could run faster than Joe at a specified heart rate – though of course Joe could push his heart rate far higher than I could, and therefore he would have left me far behind in a race.  Perhaps I was a more efficient runner than Joe at slow paces, but efficiency is less important than VO2 max for all events other than ultra-marathons. 

I started to wonder whether or not the increased severity of my asthma and my low heart rate were evidence that some non-conscious part of my brain was taking action to prevent me over-exerting myself.  On balance, this apparently hypothetical tyrannical guardian angel appears to be acting in my best interests, and in particular, is protecting my heart, but the tyranny felt as irksome as an over-protective nanny.  It seemed worthwhile to get a heart rate monitor and try to wrestle some of the control back from this over-protective nanny.

Fatigue and the parasympathetic system

I hoped to use the monitor to maximse the efficiency of my training.  However, I had not anticipated the effects of my recent illness – a protracted bout of chicken pox accompanied by various complications.   In the aftermath of a viral illness there is risk of the enigmatic condition known variously as post-viral fatigue, myalgic encephalopathy (ME), or chronic fatigue.  The name used depends on the individual’s personal investment in the problem.  Many sufferers are adamant that it has a physical cause and tend to prefer terms like post-viral fatigue or ME; while skeptics tend to say it is all in the mind and prefer the term chronic fatigue. 

I suspect that multiple causes contribute: there are predisposing factors, precipitating factors and maintaining factors.  There is little doubt that viral illness can be a precipitating factor.  Possibly a tendency towards low parasympathetic activity is a predisposing factor, although paradoxically, excessive anxiety and sympathetic activity might also be a precursor.  There is a fairly large but inconsistent body of evidence indicating that the parasympathetic nervous system can be deranged in chronic fatigue – a confusing situation encapsulated in the title of a review article by Freeman ‘ The chronic fatigue syndrome is a disease of the autonomic nervous system: Sometimes.’ (Clinical Autonomic Research vol 12, pp. 231–233, 2002).  Typically, cases of chronic fatigue show evidence of an incipient vaso-vagal attack during orthostatic testing.

Although the literature on chronic fatigue is largely to be found in journals of cardiovascular medicine, immunology or psychiatry, while the literature on over-training is confined to sports medicine journals, it is probable that the two conditions have much in common. 

I also think there is little doubt that what I suffered in mid-August was the beginnings of a bout of post-viral fatigue.  Although I had attempted to return to training fairly cautiously after my illness, my decision to persist with my plan to run a half-marathon probably led me to push myself a little too hard.  I would not describe my present problem as an over-training syndrome yet, but I think I am on the edge.

Here is the record of my heart rate during the orthostatic test when my condition reached a nadir on 18^th August, together with a more typical recording performed on 2^nd  August.

On 18^th August, during the initial 3 minutes lying-down, my mean heart rate is 51 and there are high frequency fluctuations on a time scale of around 15 peaks /minute.  During the 30 seconds following standing my pulse rises to 71 bpm but then, while remain standing, an excessive parasympathetic surge produces a fall to a mean value slightly lower than the value when lying down, at times falling below 40 bpm.  It is noteworthy that the frequency of fluctuations decreases while standing relative to lying down, indicating greater sympathetic input, though the frequency while standing on 18^th Aug is still higher than on 2^nd  August.  The increase of 9 bpm from resting to standing on 2 August is typical

How is it best to manage the situation?

The management of chronic fatigue is a hot potato.  Many sufferers maintain that exercise is harmful (see for example: http://www.empowher.com/news/herarticle/2009/08/12/top-ten-list-recovery-chronic-fatigue-syndrome.  

In contrast, the evidence from clinical trials indicates that carefully graded exercise can be beneficial (Larun and colleagues, Cochrane Database of Systematic Reviews 2004, Issue 3)   The debate is heated because of the implication that if it can be cured by graded exercise, perhaps it was all in the mind after all.  However, I think that view underestimates the amazing nature of the mind, and the brain that under-pins it.  

The mind is no less real than the immune system or the cardiovascular system.  Almost certainly non-conscious mechanisms in the mind (and its brain) act to protect us from ourselves.  It is likely that the excess of parasympathetic activity that can occur in chronic fatigue is one such a mechanism.  However, despite being clever, the non-conscious mind is not always wise, because it is dependent on the information we feed to it.  If our conscious mind reinforces the need to be protective, it is possible to create a vicious circle in which conscious and non-conscious mechanisms get cemented into an over-defensive reaction.   By judicious conscious efforts to test the limits, we might be able to train the non-conscious mind to adjust the tightness of the leash in an optimal manner.    

If so, perhaps the most effective way of preventing incipient post-viral fatigue from becoming protracted debilitating chronic fatigue is to undertake carefully graded exercise so that the non-conscious mind/brain can adjust the tightness of the leash rather than consolidate the current status and create an intractable chronic problem.

Here is a graph showing the day-by-day variation in the difference between lying and standing heart rate during the orthostatic test. 

Orthostatic increase in heart rate showing nadir on 18th August. red arrows indicate long-run days; blue arrows indicate rest days

After the nadir in mid-August, there was a fairly steady improvement.  The red arrows mark days (both before and after the nadir) when I had increased training volume up to 15Km or more (albeit at a very easy pace).  On each occasion, there was a deterioration on the following day.  The blue arrows indicate days of complete rest.  These are followed by improvement, but perhaps even more importantly, during the period including runs of gradually increasing intensity over short distances, from 25-29^th August, the trend was strongly upwards.  Over this period, the Poincare plot ( a two dimensional scatter-plot that illustrates variation in inter-beat intervals, and in particlar allows as estimate of the rapid beat-by-beat changes in interbeat interval produced by activity of the parasympathetic nervous system) revealed that increasing orthostatic rise in heart rate was accompanied by decreasing parasympathetic drive during the standing phase.

Many a slip between cup and lip.

On Saturday (29^th August) I was sufficiently encouraged by my progress that I was tempted to increase training volume.  I ran 15 Km, starting slowly and gradually increasing up to a pace around 5 min/Km, achieving an overall average pace of 5:24.  This was a mistake.  On Sunday morning, the orthostatic difference was back down to 1 bpm.  This morning (Monday) it was 2 bpm.  It was clear that I still need to take things cautiously.

I decided that instead of running today I would repeat a session on the elliptical cross-trainer which I had done in mid July, at a time when I was gradually building up the training-load after my illness.   During the session, I increased the work-rate very gradually at 4 minute intervals, starting at 35 watts and increasing to 240 watts.  When I had done this session in mid-July, I had exceeded the ventilatory threshold (where breathing become very deep and rapid) during the final two levels.  My average heart rate in the final few minutes was 157 bpm (about 98% of maximum), but it had been an exhilarating rather than demanding session.  I anticipated that despite my recent fatigue, the training I had done since early July would be enough to allow me to achieve a 240 watt output while barely exceeding the ventilatory threshold. 

I felt reasonably relaxed during the early phases, though occasional glances at the heart rate monitor indicated that my pulse was rising at a similar rate to mid-July.  And then at 200 watts, I hit a very solid wall.   Suddenly I was gasping for breath.  I could scarcely believe how difficult it was.  However, it seemed that little harm could come from a few more minutes of exertion so I pushed on for the full 4 minutes of the 240 watt level.   When I examined the heart rate recording I was stunned to see that my heart rate had stopped rising after reaching 143 bpm at the 200 watt level.  The subsequent 240 watt level had felt so difficult because there had been no appreciable increase in cardiac output despite an increase in work-rate.  In the final few minutes I must have been utilizing almost purely anaerobic metabolism. No wonder it felt difficult.

The Poincare plot confirmed that it was the parasympathetic system that had blocked further rise in cardiac output beyond the level reached at 200watts.  A comparison of the Poincare plots in mid-July and today demonstrate that the variation along the 45 degree axis of the ellipse (largely due to sympathetic activity) was very similar on the two occasions: 6.9 ms in July compared with 5.6 ms today, but the variation across the 45 degree axis had increased more than threefold from 4.0 ms  to 13.4 ms, indicative of a relatively large amount of parasympathetic activity.  The consequence of this parasympathetic drive was a false ceiling on VO2max, and the sensation of hitting a solid wall.  I wonder does this mechanism play a part in creating the wall dreaded by ill-prepared marathoners?

Poincare plots of R-R intervals over a 2 minute period during the 200 watt level in the elliptical session on 18th July and 31st August

The future

I must now steer a course between Scylla and Charybdis, the mythical monsters that guarded the Straits of Messina.   If I push myself too hard the excessive stress will evoke an even more restrictive parasympathetic defense and I am likely to end up with protracted fatigue.  However, the evidence from studies of chronic fatigue indicates that the dangers of molly-coddling myself are almost as great.  Acute post viral fatigue can become very entrenched if the non-conscious mind/brain learns that the only safe path is low intensity activity.  

Previously in such circumstances I would have been inclined to opt for slowly re-building of aerobic base with a Maffetone-style program.  However, that would not be entirely logical as I think my aerobic base is still fairly robust.  The observations of the past 10 days suggest that short, moderate intensity sessions might be more effective for promoting recovery, whereas longer runs are likely to lead to further deterioration.

As for my half-marathon plans, I will simply have to see what unfolds in the next 10 days.  The Gratze study suggests that the two most crucial things to do in preparation are tapering, and ensuring that serum potassium level is not low.   Unfortunately, one of the side effects of my asthma inhaler is a decrease in serum potassium, so there are other less fearsome but nonetheless potentially troublesome monsters circling not far below the surface as I attempt to cajole my over-protective nanny through the gap between Scylla and Charybdis.  At this stage negotiating that gap is more important than the half-marathon, but provided my orthostatic test results show a moderate degree of normalization, I am inclined to at least present myself at the starting line.

I am on the road to recovery from the debilitating illness that had incapacitated me for 4 weeks. The two charts below show the Poincare plots of R-R intervals recorded using my Polar RS800cx during 5 minutes of relaxed deep breathing while sitting, on 12th July (3 days after the resolution of symptoms) and on 18th July (9 days after resolution of symptoms).

The much greater scatter of points on 18th July demonstrates that I am now far less stressed. On 12th July mean heart rate while sitting was 60 bpm while it had decreased to 54 bpm by 18th. Even more dramatically, the overall standard deviation, which provides an indication of the overall amount of variability in heart rate, had increased from 40.1 milliseconds to 82.9 milliseconds. The standard deviation in the direction at right angles to the 45 degree line (which provides an indication of the amount of parasympathetic activity) increased from 23.8 milliseconds to 56.4 milliseconds. These numbers reveals that the variability of my heart rate had more than doubled over the six day period. The increase is due to an increase on both parasympathetic activity (which is associated with relaxation and recovery) and also an increase in variability of sympathetic activity.

I had done some easy running on 10th and 11th July, and since 12th, I have done a further 3 sessions, on each occasion running 5Km in the lower aerobic zone.

Overall, these observations are very encouraging. However, I have lost a great deal of fitness during the four weeks of illness. Today, during an easy 5Km run, I recorded 722 heart beats per Km, whereas I was recording values around 650-680 beats per Km when running at a similar pace before I became ill. Although the degree of variability is similar to that before I became ill, my average heart rate of 54 bpm when sitting today was still somewhat higher than the 46 bpm recorded prior to my illness. I think these data should be interpreted as evidence that my stress levels are back to near the pre-illness levels, but my aerobic fitness is substantially reduced. Nonetheless, the recovery of my heart rate variability suggests that I am now sufficiently recovered to resume regular training.

After much deliberation about buying a heart rate monitor capable of recording Heart Rate Variability (HRV), I have decided to be profligate, and have bought a Polar RX800cx.  I had been vacillating between a Polar RS800cx and a Suunto t6r.  For the purpose of measuring HRV, the Polar RS800cx and the Suunto t6r have very similar capability.  Both devices record R-R interval (the interval between the ventricular contraction of consecutive heart beats), and either can be used to provide the raw data required by the Firstbeat software which I have discussed on several recent postings.  This software computes a stress/ recovery index which promises to provide a sensitive indicator of impending over-training.  This stress/recovery index is based on estimate of the balance between activity of the parasympathetic nervous system (which promotes recovery) and the sympathetic nervous system (which promotes fight or flight).

When it came to the final decision about which device to buy, I was swayed by the fact that RS800cx comes with a stride sensor that appears to provide a reliable measure of cadence.  I am very interested in assessing my cadence when running, but a discussion of the reasons for my interest will have to wait for later posting as my first objective was to see how useful R-R data might be for measuring stress levels.

The Polar Own Optimizer

Although I have focused mainly on First beat software in recent weeks, the software that comes with the Polar RS800cx does include a utility called Own Optimizer, which assess stress levels on wakening in the morning.  Unfortunately, the information provided in the manual provides little scientific justification for the Own Optimizer.  As far as I can gather, Own Optimizer is based largely on the changes in both heart rate and HRV in response to rising from sitting to standing.  In principle such measurements might provide a sensitive measure of the degree of withdrawal of parasympathetic nervous activity and increase in sympathetic activity associated with the mild challenge of standing-up. Therefore, I will be curious to experiment with Own Optimizer, but the output of Own Optimizer is difficult to interpret unless one has baseline data recorded while in a relaxed state. There is little point in me trying out Own Optimizer until I am fully recovered from my recent episode of illness.  Nonetheless, I hope eventually to compare Own Optimizer with the Firstbeat stress/recovery index.

Back to the Poincare scatter plot

Meanwhile, I exported the R-R data from my new RS800cx and subjected it to the same Poincare analysis which I had presented in my post on 26^th June.  The Poincare analysis requires the production of a scatter plot which can be produced easliy using software such as Excel.  Interpreting  the scatter plot taxes the grey cells, but the effort is probably worthwhile.

The Poincare analysis is based on a scatter plot in which each heart beat is plotted on the x-y plane with the x-coordinate equal to the interval between the preceding beat and the beat of interest, while y coordinate is equal to the interval between the beat of interest and the following beat.   A heart beat for which the preceding inter-beat interval is equal to the subsequent inter-beat interval must lie on a line that represents the equation x=y.  This line slopes upwards and to the right at 45 degrees, as shown in the figure below.  Strong parasympathetic activity is associated with large beat by beat variability in heart rate, so consecutive interbeat intervals will differ substantially in duration and the  points representing the heart beats  will lie at a substantial distance for the 45 degree line. 

Conversely, if inter-beat interval varies slowly (over a time scale long compared with the average inter-beat interval) then each heart beat will be represented by a point near the 45 degree line, though the slow variation will cause the location of the points representing the heart beats to wander along the 45 degree line.  Slow fluctuations are largely due to sympathetic nervous activity, though there is evidence that parasympathetic activity can also contribute to slow variations – however for the present purpose, let us assume that sympathetic nervous activity is mainly responsible for slow variation, resulting in a spread of points along the 45 degree line, while parasympathetic activity is responsible for rapid variation that causes a spread of points away from the 45 degree line.

 As I described on 26^th June, if there is a good balance between sympathetic and parasympathetic activity, the scatter plot should produce a cluster of points that looks like a swarm of bees the spreads out both along the 45 degree line and away from the 45 degree line. If we draw an ellipse that captures most of the points, this ellipse will be almost circular.  Conversely, if the person is stressed, so that there is an excess of sympathetic activity, the scatter plot will produce a cigar shaped cluster extending along the 45 degree line.  In the data which I had recorded using my ‘home-made’ ECG device before my recent illness, the scatter plot had exhibited a large spread away from the 45 degree line in addition to a large spread along the line.  The ellipse that embraced most of the points was pleasingly round.

 Here is a comparison of the scatter-plot for data recorded today (using my new RS800cx)  with data recorded before my recent illness.  Both sets of data were recorded while sitting in a relaxed state, breathing slowly and deeply.  The pre-illness recording was in fact made at around 6pm at the end of a day at work, while today’s recording was made in the early afternoon after a relaxing Sunday morning.  Thus, if all other circumstances were the same, today’s plot might have been expected to show an even more favorable balance between parasympathetic activity and sympathetic activity.  However, all other circumstances were not the same.  Today, I am in the fourth day of convalescence after a peculiar and debilitating illness that lasted almost 4 weeks.

Poincare scatter plot pre- and post illness

There are two striking differences.  First, the cluster of pink dots presenting today’s data has moved down and to the left, indicating that the average inter-beat interval was shorter.  A shorter inter-beat interval corresponds to a faster heart rate.  Before my illness, my average heart rate was around 46 beats per minute.  Today’s value was 59 beats per minute. Secondly, the ellipse that embraces the majority of the points is thinner – somewhat more like a cigar.  Today’s data reveals substantially reduced heart rate variability, especially a reduction of the parasympathetic activity that produces rapid changes in heart rate and scatters the points far from the 45 degree line.

Occasional parasympathetic surges

There are a few points that are outside the ellipse that embraces the general trend.  Several of these points represent heart beats for which a preceding short inter-beat interval was followed by a longer than usual inter-beat interval (causing a large displacement above the 45 degree line).  In fact these points represent a sudden drop in heart rate from around 58-62 beats per minute to 52-55 beats per minute. It appears that I was experiencing occasional surges of parasympathetic activity.  These surges were also apparent when I examined an even longer recording, so I suspect that they are not just random chance events but in fact represent some fairly consistent pattern of autonomic nervous activity.  I do not have an explanation for those occasional sudden surges of what appears to be parasympathetic activity.

The main conclusion

However, the main conclusion is very clear.  My recent illness has left me in a quite stressed state – at least compared to my relaxed pre-illness condition.  In fact, although today’s recording reveals a marked deterioration, it is not too bad for a 63 year old, so there is no reason for me to be too alarmed.   However, it would probably be unwise for me to resume vigorous training until the scatter plot of data recorded in a resting state returns to something more like the widely dispersed shape exhibited in my pre-illness data.

The apparent sensitivity of the Poincare scatter-plot to stress level makes me wonder how useful if might prove to be as a measure of training stress.  Once I have recovered fully, it will be interesting to compare the scatter plot following a hard training session (‘over-reaching’) compared with that following easier training sessions.  Maybe the Poincare scatter plot of data record during relaxed deep breathing will be as informative as either Polar’s Own Optimizer or the stress/recovery index computed by Firstbeat software.  Whatever the relative merits of the different ways of assessing autonomic imbalance from HRV data, it appears that HRV is a sensitive indicator of one’s internal milieu.

I have been blogging a little more frequently in the past week or so because I have been ill, and therefore not running.  I have been exploring issues related to over-training and heart rate variability on my blog because one possibility is that I had become ill because of over training.  At this stage I am puzzled.

A peculiar illness

First an outline of the illness: it started over three weeks ago with an exacerbation of my long standing inflammatory arthritis; then became an acute fever with a temperature of  101-104 degrees F. for a few days; then what appeared to be chicken pox with  fairly typical skin vesicles, and  most distressingly, severe mouth ulceration. I have largely been living on ice-cream and cool fluids for over a week.  This morning, I woke at 3:30 am with a new crop of painful vesicles in my mouth, a painful throat and a mild asthma attack.  At this stage I am a little worried that the problem will extend more deeply into my lungs, though as I sit at my desk typing this I do not feel seriously ill.  Maybe it’s just chicken pox and a few incidental problems, though since I had chicken pox as a child, it’s all a bit mysterious.

Could this peculiar illness be a consequence of over-training?  At this stage I think it is very unlikely.  As I have been discussing in recent postings, there is good evidence for regarding the balance between sympathetic and parasympathetic nervous activity as a useful measure of recovery from training.  As I posted last week, my heart rate variability before I became ill indicated a good balance between parasympathetic and sympathetic activity. Since I have been ill, I have not recorded heart rate variability but simple tests such as the orthostatic test (change in heart rate on standing) indicate there has been a small shift from parasympathetic to sympathetic activity.  This is only to be expected with the degree of illness I have experienced.  Nonetheless, I can still get my heart rate down to the low 50’s by relaxed rhythmic breathing, so the evidence suggests I still have reasonably good parasympathetic control. If maintaining a good balance between parasympathetic and sympathetic activity is a sign of good recovery from training, I have been recovering well.

Could my illness be due to immune suppression produced by the steroid inhaler I use for my asthma?  My doctor thinks that is very unlikely. So the situation remains a mystery,   At this stage I do not know when I will get back to running.

The overall balance sheet

Though at the moment I am not well, it is also important to keep in perspective the overall balance sheet with regard to my health since I recommenced running.  Let’s start with the negative side of the balance sheet.  The one definite deterioration has been in my asthma.  Although I have suffered mild asthma since childhood, I had never needed treatment until a year or so ago.  It is possible that getting cold air into my lungs when running has exacerbated that problem. My arthritis presents a different story.  It had also been a mild problem since childhood but had started to become more of a problem as I approached middle age. In particular my right knee and the metatarsophalangeal joints in my feet were starting to be troublesome.  But contrary to expectations, those problems have greatly improved since I started running. The recent flare-up of arthritis was I fact very minor.  Most importantly for my general health, I think the decrease in my resting heart rate, from around 60 a few years ago down to the mid 40’s, is an indication that my heart is much healthier as a result of running.  So I think the balance sheet is positive.

Maintaining the balance

Meanwhile, I still continue to be fascinated by the question of how best to monitor training so as to maximize both my health and my running performance.  Even though there is little to suggest recent over-training, my experience of the past couple of years has demonstrated that I am now less able to cope with heavy training than forty years ago.  Maybe that is an inevitable consequence of aging.  But if I accept that, it becomes all the more important to develop good strategies for optimizing training level.

My overall conclusion is that training vigorously is almost certainly the best way to remain healthy into old age, but finding a good way to judge just how vigorously to train is the challenge.   I am also inclined to think that for an athlete of any age, the challenge is similar.  Finding the optimum balance between stress and recovery is likely to be the recipe not only for achieving for good general health but also for maintaining the consistency of training necessary to achieve one’s peak performance.  I just hope I can get back to running soon, though I might have to wait a year or two to achieve my M60 peak performances.

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.

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.

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.