In recent posts I have discussed the evidence regarding the relative merits of high intensity training and high volume training.  The evidence demonstrates that both approaches are effective for increasing aerobic capacity.  Both will develop capillaries and mitochondria in heart and skeletal muscles.  High intensity training allows a more efficient use of time, which might be the decisive feature for an amateur athlete with family and work commitments, though in general, high intensity work-outs are tougher and require greater determination. 

Potential benefits of mixing high and low intensity

Furthermore the two approaches are each attended by risk of injury or over-training.  However it is probable that the risk of injury and over-training associated with the two intensities of training arise from somewhat different stresses on the body.  High intensity training produces greater forces on the musculo-skeletal system, but also produces greater increases in anabolic hormones, whereas high volume training produces greater increases in catabolic steroids such as cortisol, which can promote destruction of muscle if excessive.  On the other hand, there is relatively little evidence suggesting that a high intensity session undoes the benefits of a preceding low intensity session or vice versa.  Therefore, my provisional conclusion is that the best approach is a program that includes a mixture of high intensity and low intensity (high volume) sessions, on the grounds that such an approach is likely to achieve a good balance between stimulation of catabolic and anabolic hormones. This remains unproven but is at least plausible.

What about the mid-zone?

However, this leaves unanswered the question of whether or not training sessions that fall in the mid-zone between high intensity and low intensity (but high volume) are of much value.  Surveys have shown that elite athletes tend to avoid the ‘grey’ zone between high intensity and low intensity,  For example, the study by Seiler and Kieland found that elite skiers do about 75% of their training at low intensity and 15-20% at high intensity with only around 5-10% in the mid intensity range  (Scand J Med Sci Sports. 16(1):49-56, 2006).  Previously the French exercise physiologist, Veronique Billat, had reported similar proportions of time in the different training zones in marathon runners (Med. Sci. Sports Exerc. 33:2089–2097. 2001)

The Esteve-Lanao study

It was therefore with great interest that I read a report on a study by Jonathan Esteve-Lanao and colleagues (Journal of Strength and Conditioning Research, 21(3), 943–949, 2007), which had been pointed out to me by Simon in a comment on my post comparing high and low intensity training on October 25^th.   Esteve-Lanoa is a coach in Madrid who had previously published findings demonstrating that the proportion of training time spent in the low intensity zone was a strong predictor of race performance (Med Sci Sports Exerc. 37(3):496-504, 2005.) 

In the more recent study published in 2007, he allocated a group of well-trained sub-elite athletes to one of two programs for a period of 5 months: one program included more low intensity training than usual for this group of athletes; the other involved less low intensity training and more mid-intensity training.  Both groups performed the same amount of high intensity training.  Intensity was assessed according to proportion of training time with heart rate within low, mid and high intensity zones defined relative to the ventilatory threshold (VT) and respiratory compensation threshold (RCT). 

Defining the zones:  VT is the first appreciable step in respiratory effort as work load increases, and corresponds to the threshold described as VT1 by some authors (eg Dekerle and colleagues) or aerobic threshold by others.  It is the highest work rate that can be fueled virtually entirely via aerobic metabolism. At higher work rates, appreciable anaerobic metabolism occurs, and lactate level rise appreciably above resting values.  The increased acidity in the blood causes the noticeable rise in respiratory effort necessary to remove more carbon dioxide, thereby compensating for the lactic acid by reducing the acidity due to dissolved carbon dioxide.   Lactate is removed by organs such as liver and heart which can use lactate to generate energy.   As work rate rises further, a stage is reached beyond which the body cannot remove the lactate as fast as it is produced.  At this stage lactate level and acidity rises rapidly.  There is a major drive to increase respiratory effort in an attempt to compensate for the acidity.  This is the respiratory compensation threshold (RCT), which is also known as VT2 or anaerobic threshold.   Thus, in the study by Esteve-Lanao, low intensity training at a heart rate below that corresponding to VT is virtually entirely aerobic.  In the mid-intensity zone between VT and RCT, training involves some anaerobic metabolism but the body can cope with the rate of lactate production and lactate level remains only a little above resting value.  In the high intensity zone above RCT, a large proportion of the energy is generated by anaerobic metabolism and the level of lactate rises to high levels, compelling the athlete to make a very strong respiratory effort in an attempt to deal with the rising acidity. 

The results:  In the group assigned to an increased amount of low intensity training, the amounts of times in heart rate zones corresponding to low, mid and high intensity training were in the ratio 80:12:8 (i.e. 80% low intensity).  For the group assigned to decreased low zone training, the ratio was 67:25:8  (i.e. 13% less in the low zone, replaced by 13% more in the mid-zone).  In both groups VT occurred at approximately 67-68% of VO2max, while RCT occurred at approximately 87-88% of VO2max.  The outcome of training was assessed by comparing time recorded in a 10.4Km cross country race before and after the 5 month period of training.  The group who had HR in the low zone for 80% of the time improved by 7.5% while the group who had HR in the low zone for only 67% of training time, improved by 5%.  The difference between groups in amount of improvement was statistically significant.  It should be noted that the individuals with HR in the low zone for 80% of the time spent more hours training (average 100 hours over 18 weeks compared with average 75 hours in the group with HR in the low zone for 67% of the time), but the total load (volume x intensity) was similar in the two groups. The authors conclude: ‘These results provide experimental evidence supporting the value of a relatively large percentage of low-intensity training over a long period, provided that the contribution of high-intensity training remains sufficient.’

It is crucial to note that even the group with 80% low intensity training performed a substantial amount of demanding work. They did 2 intense sessions per week in many of the weeks, in addition to regular weight training, and also running 5 cross country races (2 x 5Km and 3 x 10Km) not including the final assessment. Nonetheless, I think the practical conclusion is that training in the mid-zone produces less benefit that a similar work load (volume x intensity) in the low zone provided the program includes sufficient high intensity work.

It should also be noted that the amount of time spent with heart rate corresponding to the mid-zone intensity does not correspond exactly to the amount of time spent working in this zone.  Typically in an interval session, it takes from 1 to 2 minutes for HR to reach the high intensity zone (due to buffering by myoglobin) during high intensity epochs, and it takes 1 to 2 minutes before HR falls back to low zone level during the recovery.  When I do 1 Km intervals, my heart rate is in the mid-zone for more than half of the session despite the fact that I do not spend any time running at a mid-zone pace.   To achieve 8% of training time in the high intensity zone typically would require about 15% of sessions to be high intensity sessions.   

On the whole this appears to be a sensibly designed and well executed study.  The main concern I would raise is the fact that Esteve-Lanao’s previous study published in 2005, in which he found that the amount of low intensity training predicted race performance, might have inclined him to have greater faith in low intensity training.  He coached all the athletes in the study reported in 2007.  There is evidence that having faith in a particular training program influences the physiological benefits from that program.  It is therefore possible that coach’s confidence in the low intensity program influenced the outcome.   It is because of unconscious influences of this sort that double-blindness is regarded as so important in trials of medical treatments.  Nonetheless, despite this potential short-coming, I consider that this study provides moderately strong support for the proposal that mid-aerobic ‘grey zone training’ is a limited value.

As described in my post on 25^th October, the events of the past summer indicate that I need to plan a long term campaign if I am ever to recover a level of fitness equivalent to that of my younger days, after allowing for the anticipated rate of decline with age illustrated by the WAVA charts.   My goal is to run a ‘good’ marathon in 2012, perhaps aiming for a target time in the range 3:15 to 3:30, and to continue to enjoy running for many years after.

What needs to be developed, and how can the required development be achieved? 

1)    Aerobic capacity of leg muscles: the ability to generate energy for muscle contraction by aerobic metabolism is crucial. The aspects of aerobic metabolism that can be improved by training are:

a.  Delivery of oxygen to the muscles – the number and size of capillaries increases when there is demand for increased delivery of oxygen to muscles;  development is likely to continue over many years provided the there is continuing demand for increased oxygen delivery.   Both low intensity and high intensity training are effective.  The study by Ingjer (J. Physiol. Vol  294, pp. 419-432, 1979) reported an increase of 28.8% in the number of capillaries per muscle fibre after 24 weeks of a high intensity program that included two interval sessions per week in addition to 3 sessions of continuous running for 45 minutes at a work rate ranging from 50 to 90% of VO2max.

 b. The number of mitochondria in type 1 (slow twitch) and type 2A (aerobic fast twitch) fibres. The mitochondria are the sub-cellular organelles containing cytochrome oxidase, the key enzyme in aerobic metabolism.  Dudley’s studies of rats (J Appl. Physiology, vol. 53, pp. 844-850, 1982), discussed in my post on 25^th October, demonstrate that increase in cytochrome C is achieved most efficiently for both type 1 and type 2A fibres at high intensity running at above lactate threshold.  Similarly, in the case of humans, the study by Gibala and colleagues (J Physiol Vol 575, pp 901-911, 2006) suggests that high intensity training is the most efficient for producing increases in muscle oxidative capacity.

Although the evidence suggests that the most efficient way to increase capillary density and number of mitochondria in skeletal muscle in the short term is via fairly high intensity running (above lactate threshold) there is no clear evidence that the benefit of such high intensity training continue to accumulate over a period of several years.  I am not aware of any systematic scientific studies that have compared groups of athletes undergoing different training regimes extending over several years. 

There are very few elite athletes who are reported to have shown continuous improvement over many years of predominantly high intensity training.  Individuals such as Gordon Pirie, who did a large number of high intensity interval sessions, had a relatively brief period at the top.  In 1956 he broke the world 3000m record twice, and won a silver medal in the 5000m at the Melbourne Olympics, but he never reached such heights again.  Emil Zatopek was a dominant force for somewhat longer winning a gold medal in the 10,000m London in 1948 and three gold medals in Helsinki in 1952, but it is probable that his famous high intensity sessions (e.g. 50×400m) were run at a relatively modest pace – perhaps around 10K pace – as reported in a comment on my blog by Ewen on 31^st March 2009 . 

In the absence of observational evidence, it is necessary to rely on our understanding of physiological mechanisms.  Potentially the most important issue is oxidative damage due to free radical production.  Both aerobic and anaerobic exercise result in the production of free radicals that have the potential to damage tissue, but provided the amount of exercise is not excessive, the body’s natural defenses can cope.  However both excessive intensity and excessive volume can result in the natural defenses being overwhelmed (Fisher-Wellman and Bloomer, Dynamic Medicine, vol 8, 2009, doi:10.1186/1476-5918-8-1)  In light of this evidence I think that the best strategy to produce continued improvement in aerobic capacity over a period of several years, is likely to be a compromise.  I plan to do an a moderate amount of interval training near to lactate threshold or a little above, but will balance this with an approximately equal amount of low to mid –aerobic running; and some non-demanding exercise focused on improving flexibility and proprioception.  

2) Increased capacity of the heart to pump blood.  Cardiac output is the product of stroke volume and heart rate. Unfortunately the decrease in maximum heart rate with age is one of the major contributors to deterioration in maximum rate of oxygen utilization with age, and there appears to be little that can be done to prevent this.  Stroke volume is determined by the difference between the volume of the left ventricle at the beginning and end of ventricular contraction (systole).  Similarly to the situation with training to increase aerobic capacity of muscles, the evidence indicates that high intensity interval training is the most efficient way to increase stroke volume.   The study by Helgerud and colleagues from Trondheim in Norway (Med Sci Sports Exerc. 39(4):665-71; 2007), which I described in some detail in my post of 23^rd June 2009 demonstrated that 4x 4 min of running at 90-95% HRmax followed by 3 min of active resting at 70%HRmax, 3 times per week for 8 weeks produces a greater increase stroke volume and also increase in VO2 max than the same number of sessions of either long slow distance running at 70%of maximum heart rate, or tempo running at around lactate threshold. 

However, as in the case of aerobic development of skeletal muscle, the goal of producing continuous development over a period of years must take account of the risk of free radical damage, and I think the same compromise program that balances intensity and volume, non-demanding exercise, and rest is likely to be optimal. 

3) Leg muscle strength and power:  Although I have never formally tested my leg muscle strength, I know from my reduced ability to step upwards onto a chair while carrying a heavy object  that my muscle strength has decreased with age.  My reduced stride length when sprinting confirms this loss of strength and power.  My current time for 100m is 18 sec. I never recorded a 100m time as a youngster, but could certainly run a 400m in much less than 60 sec, so I have clearly slowed down when sprinting and this is almost certainly due to loss of muscle power.  Running entails eccentric contraction of quads, hams and calf muscles.  However, developing eccentric muscle strength presents problems, because eccentric forces tear muscle fibres.  The most efficient way to increase strength of eccentric contraction is plyometric exercise, but the sharply applied stretching of muscles during plyometrics causes extensive damage, which is also likely to produce production of free radicals and a risk of long-term damage (Bloomer RJ & Goldfarb AH. Canadian Journal of Applied Physiology, 29(3): 245–263, 2004.)   Therefore, I will engage in weekly strength training, employing exercises that entail moderate eccentric stress, and very sparing amounts of plyometric exercise.

4) Neuromuscular coordination:  In recent years I have worked on developing a style of running that I believe is efficient and fairly safe – described in the pages ‘Running – a dance with the devil’ in the side bar of my blog.  This style is closely related to Pose, but I have tried to avoid what I perceive as the problems with Pose.  I have not yet focussed on applying this style to faster running.  In the near future, I will spend a session per week practicing this style of running at ‘near sprinting’ pace, but over short distances and with adequate recovery to minimize exhaustion. 

Other metabolic and musculo-skeletal developments

There are many other metabolic developments, such as increased ability to store glucose; to burn fats; to metabolize lactate, and musculo-skeletal developments such as resilience of connective tissues that I anticipate are best developed within the context of a comprehensive program focusing on the four key elements described above   

The program

I plan a periodized program comprising periods of several months duration within which I will spend several sessions a week focusing on the development of specific aspect of fitness, while maintaining a continuous background of aerobic development.  In addition I will spend one or two sessions per week on core strength, balance and proprioception.

Taking account the above considerations, here is my proposed program for the next 4 months:

Specific goal: increasing leg muscle strength and neuromuscular coordination.  The program will include the following sessions:

1) body-weight exercises that entail moderate eccentric load on the major leg muscles: hams, quads, gastrocnemius, soleus, peroneals, gluteals and tensor fascia lata (1/2 hour per week);

2) short hills (approx 90 seconds, 4-8 reps at  ¾ pace effort) on alternate weeks.

3) running style sessions:  mainly drills and short stride-outs focusing on a relaxed style.

Aerobic and cardiac development:

1)      Two interval sessions per week on the elliptical cross trainer.

2)      One long(ish) run: approximately 15Km at whatever pace appeals to me on the day.  I anticipate that these runs will mainly be progressive runs starting in the low aerobic zone and increasing to mid aerobic or upper aerobic zone for the final few Km, though on some occasions I will include 5-10 Km of fartlek within the 15 Km run.

Core strength, balance and proprioception

1)      body-weight exercises designed to improve core strength (1/2 hr per week)

2)      exploration of Yoga postures suitable for development of balance, flexibility and mental focus (1/2 hour per week)

This program entails 7 or 8 sessions of quite diverse content, per week, requiring a total duration of 4 ½ to 5 hours.  The amount of running in this 4 month period is intended to be modest, including one weekly 15Km run; a weekly running style session; and a short hill session on alternate weeks, while I focus on leg strength and neuromuscular coordination.  I anticipate that the most demanding sessions will be the elliptical interval sessions.   These will provide a substantial work-out for the cardiovascular system but due to the fact that the elliptical action involves no impact and relatively little eccentric contraction of leg muscles, the stress on the legs is relatively mild.

I will aim to do at least 80% of the scheduled sessions, but will occasionally substitute other activities such as hill walking, swimming, cycling or kayaking, as the opportunities present themselves

My provisional plan beyond this 4 month period is to devote 2 months to specific preparation for a 10K race in spring.  The major change will be the replacement of some of the elliptical sessions and strength sessions by interval and tempo running sessions.  Then during the summer of 2010, I will prepare for a half marathon in autumn.

As the daylight hours shorten and we enter the final few weeks of autumn, I am thinking about goals for the coming months.  Looking back, it has been a frustrating summer.  A debilitating illness in June and July torpedoed my preparation for the Robin Hood half marathon in September. My eagerness to determine whether or not I could recover sufficient fitness by September led to a series of problems, the most serious of which was intense over-activity of my parasympathetic nervous system that clamped my maximum heart rate at around 142 bpm in mid-August.  On September 13^th, I lined up for the race in a seriously under-prepared state.  My aerobic fitness was not too bad, but I had not prepared my muscles for the rigors of a half marathon race.  Perhaps it was unsurprising that I tore a hip adductor while making a sharp turn across an uneven patch of roadway at about 6 miles.  I did manage to complete the 13.1 miles with a markedly shortened stride and virtually no airborne phase, in a time a little over 103 minutes.  I was pleased that I had managed to get to the finish, and I learned a few things along the way, but overall it was a very frustrating summer. 

Among the things the summer has emphasized is that acquiring aerobic fitness is only a small part of what is required.  If I am going to recover the ability to race at paces in any way comparable to the paces I used to run in my youth, after allowing for the effects of 4 decades of aging since that time, I need a long term plan.  I would like to run a good marathon again, but because I currently work about 50-60 hours per week, there is no possibility that I could do enough training to do justice to a marathon in the near future. 

I plan to reduce my working hours substantially in 2011.  So my goal is a ‘good’ marathon in 2012, but what could be described as a ‘good’ marathon?  Using the WAVA adjustment for age, my races of 40 years ago indicate that, all being well, I might be capable of a marathon time around 3 hours in my late 60’s.  However, several minor ailments which I have had since childhood and which caused minimal problems in young adulthood, have been much more troublesome since my fifties, so a 3 hour marathon is clearly out the question for 2012. For the time being I will set a provisional target in the range 3:15 to 3:30, and refine this target more precisely in light of what appears plausible as 2012 approaches. 

How should I prepare myself?  The major debate in endurance training is the debate between focus on high intensity and high volume training.

High intensity

The father of high intensity training was the German coach and cardiologist, Woldemar Gerschler, who developed the concept of interval training: bursts of anaerobic activity separated by brief recovery epochs.   This approach led in a fairly direct path via coaches such as  Franz Stamfl, to Roger Bannister’s demolition of the 4 minute barrier for the mile in 1954.   The parallel development of a similar approach led Emil Zatopek to gold medals in the 5000m. 10,000m and marathon in Helsinki in 1952, though it might be argued that Zatopek combined high intensity with high volume. 

More recently, the Furman Institute have developed a program based on only three running sessions per week entailing high intensity with modest volume.  The Furman program is supported by scientific evidence about the most efficient way to enhance aerobic metabolism, and the studies performed by the Furman Institute provide clear evidence that the program works in practice.  In an article in Runners World in Feb 2006, Amby Burfoot, reported that 15 of a group of 25 amateur runners who undertook the Furman program in preparation for the Kiawah Island Marathon while maintaining their usual commitments to jobs and family, set personal best times.

The paces specified for the three weekly runs in the Furman program: an interval session; a tempo session; and a long run, are all very demanding.  My own judgment is that the program places a little too much emphasis on aerobic development and not quite enough on development of endurance, but I have no doubt that for a runner with the determination to adhere to the program, it offers a good prospect of achieving the target time.  At first sight, the demanding paces might appear to carry a substantial risk of injury.  However, the fact that there are only three running sessions per week provides a fairly generous amount of time for recovery between sessions, thereby minimizing the cumulative fatigue that predisposes to injury.  In the Runners World article, Amby Burfoot reported that there was only a modest injury rate among the group of 25 runners in the Furman marathon study in 2004.   Injury forced one to withdraw from the program, and minor injury led three to drop from the marathon program to the half marathon program.

Because I think the Furman program does not place enough emphasis on endurance, I consider that it is only a useful program in the final four months of preparing for a target race once a sound base has been established.  I do not consider it is suitable  as the mainstay of a three year campaign, though I will reconsider it as I prepare for a few targeted half-marathons along the way.  I might consider a modified version of the program in the final phase of the campaign in 2012  but perhaps I should not make too many assumptions this far in advance 

High volume

The father of the high volume approach was Arthur Lydiard.  He promoted periodization of training with the major emphasis on the base building period, in which most the important feature was running about 100 miles per week at ‘a good aerobic pace’.  The spectacular tally of Olympic gold medals by Lydiard’s protégés, Peter Snell (800m, Rome 1960; 800m and 1500m, Tokyo 1964); Murray Halberg (5000m, Tokyo 1964), Lasse Viren (5000m. and 10000m, Munich 1972); and Pekka Vasala (1500m, Munich 1972) leaves little doubt that Lydiard’s approach can be extremely effective.  

More recently, coaches such as Hadd have reformulated Lydiard’s approach for an era in which heart rate monitors have facilitated a scientific approach to high volume training.  While Hadd’s approach is based on the sound practical foundation developed by Lydiard, and incorporates some sensible suggestions about using the HRM to monitor progress, ironically, his science appears to be based on a mis-reading of the scientific literature.  He appears to have mis-interpreted Dudley’s studies of rats (’Influence of Exercise Intensity and Duration on Biochemical Adaptations in Skeletal Muscle,’ Journal of Applied Physiology, vol. 53, pp. 844-850, 1982).  Dudley subjected laboratory rats to 8 weeks of training involving running on a treadmill 5 times per week at various intensities and for various durations.  He measured the increase in cytochrome oxidase, a group of enzymes located in mitochondria, that catalyze the final steps of oxidative metabolism.  The amount of cytochrome oxidase provides a good measure of aerobic metabolic capacity. Examination of Dudley’s data clearly demonstrates that the gains in aerobic capacity increased with increasing intensity of training up to VO2max, not only in muscles dominated by fast twitch fibres, such as white vastus, but also in muscles with predominant slow twitch fibres, such as soleus.  It is only at supra-maximal intensity levels above VO2max that there is any evidence of a lesser rate of improvement in aerobic capacity with increasing intensity.  Furthermore, at these supramaximal levels the total duration of training was less, and the lesser improvement in aerobic capacity might reasonably be attributed to decreased duration of running rather than inhibition of aerobic development.

It is not only evidence from studies of rats, but also the majority of evidence from studies of humans demonstrates that training intensities in the range between the anaerobic threshold (at which lactate accumulation accelerates) and VO2max (beyond which heart rate does not increase despite increasing power output) are effective for improving aerobic capacity.  In the study by Gibala and colleagues comparing 6 sessions of high intensity sprint cycling consisting of 4 to 6 30second sprints with 6 session of endurance training consisting of 90-120 minutes of cycling at 65% of VO2max, over a two week period, similar improvements in performance; muscle oxidative capacity; muscle buffering capacity; and muscle glycogen content were produced even though the total training time commitment was only 2.5 hours for the sprint training compared with 10.5 hours for the endurance training (J Physiol Vol 575, pp 901-911, 2006). Unfortunately, Hadd’s interpretation of Dudley’s data appears to have contributed to a fear among his disciples that exceeding lactate threshold during training will damage the development of aerobic capacity.   I believe this fear is unfounded.

It is also important to note that both Lydiard and Hadd advocate that a substantial proportion of training should be near the upper end of the aerobic zone.  Lydiard refers to running at a ‘good aerobic level’ and recommends the use of three different intensities that span the aerobic range, with several runs a week at the highest of these levels – a pace he designates as  ¾ pace.  As discussed in my post on 9^th April 2009, Lydiard’s ¾ pace corresponds approximately to lactate threshold pace.  Similarly, except in weeks in which the weekly mileage is increasing substantially, Hadd typically recommends two runs per week at heart rate that is about 10 bpm below the lactate threshold value.  While I think that Hadd’s science is questionable, I think that in practice, many of his recommendations for training have great merit.

How do African runners train?

The current dominance of African runners, including Kenesa Bekele, world record holder for the 5000m and 10,000m, and Haile Gerbselassie, world record holder for the marathon, suggests that they must be training effectively.  It is probably simplistic to assume that all African distance runners train similarly, but nonetheless, the bulk of the evidence suggest that many do a large amount of their training at a pace near to lactate threshold.  In a study comparing black South African runners with whites, Tim Noakes and colleagues found that the black and white runners had similar average weekly running volume (60 miles per week) but the black runners did 36% of their running at  above 80% of VO2max, while the white runners did only 14% of their running above this level (Journal of Applied Physiology, vol. 75, pp.1822-1827, 1993).  However it was not simply a matter of the black runners trying harder.  The black runners produced lower levels of lactate when running at a specified intensity.  Most notably they exhibited 32% lower blood lactate concentration when exercising at VO2max.  Furthermore, they were able to sustain an isotonic contraction at 70% of maximal force for about twice as long as the white runners, despite having a similar proportion of high endurance type 1 (slow twitch) muscle fibres.  This suggests that they had a much greater degree of development of the aerobic capacity of their type 2A fibres.   In my mind, the most plausible explanation is that many years of running at paces in the upper aerobic zone had produced great development of aerobic capacity, especially of type 2A fibres, allowing them to maintain training paces at or above 80% of VO2max without undue stress.

Thus, it appears that African runners dominance is due at least in part to doing a higher proportion of their training  at fairly high intensity (eg 80% of VO2max), but there is an important caveat: the African runners produce a lower level of lactate when training at high intensity.  This is consistent with anecdotal reports that elite African runners train hard but avoid remorselessly punishing their bodies.  Furthermore, anecdotal evidence suggests many have been running since childhood and it is likely that this has provided a crucial foundation.  It might be dangerous to assume that a runner with only a few years of regular training could safely do large volumes of training near to lactate threshold.

So which is better: high intensity or high volume?

It is clear that both high intensity and high volume approaches can produce improved aerobic capacity. In a runner with moderate baseline fitness but under-developed aerobic capacity, either approach will lead to improved performance.  Perhaps the most important issue is avoiding injury.  The high power output required for high intensity running places great acute stresses on muscles, but cumulative fatigue associated with high volume training can result in failure to mount a well integrated reaction to an unexpected jolt, and lead to tearing of an already exhausted muscle.  Looking back over the years, I can attribute approximately the same number of muscle injuries to inadequate preparation for increase in volume as to inadequate preparation for increase in intensity.    

At elite level, the distinction between the programs lessens, as the choice is between high volume with fairly high intensity (eg a substantial proportion at tempo runs at 80% of VO2max) on the one hand, and fairly high volume including a substantial number of high intensity interval sessions, on the other.  Either of these options is probably only feasible for individuals with a very well established base level of fitness.  The evidence from laboratory studies suggest that aerobic fitness can be increased most efficiently by training at high intensity, and therefore a program with a substantial number of anaerobic interval a sessions is probably the most efficient way to increase aerobic fitness.   However, while aerobic fitness is crucial for distance running, it is not the only thing that matters.  The current dominance of African distance runners suggests that high volume at fairly high intensity (eg mainly near lactate threshold) might be preferable, though my own opinion is that years of running, starting in childhood, is the major factor accounting for the success of African runners.

My own younger days

I was never an elite athlete, although I suppose I could have reasonably described myself as a sub-elite marathon runner, with my best times in the range 2 hours 20 min to 2 ½ hours.  Perhaps surprisingly I have no precise record of my best races, maybe because I did not consider myself a serious athlete.  During my running ‘heyday’ I was actually more interested in mountaineering.  Insofar as I trained systematically at all, I aimed to run moderately large volumes (occasionally up to 100 miles per week) at a ‘good aerobic pace’.  I used to consider that there was little point in running any slower than 6 minute mile pace.  I preferred to spend my time walking in the hills or climbing mountain rather than running slowly.   So perhaps my training could be classified as Lydiard style though I rarely did the high volumes recommended by Lydiard.  On the other hand, I did some tigerish hill walking and mountaineering.  The other point to note is that like some of the Africans, I ran to and from school as a youngster, and during my teens, I simply regarded running as a normal form of locomotion.  I also played a lot of football and basketball.  But that was a long time ago.

The risks of too much training

Not only does training present a risk of acute injury but also a risk of overtraining.  There are two forms of overtraining : the sympathetic and the parasympathetic.  These are characterized by impaired performance accompanied by psychological a features such as fatigue and low motivation; together with a complex array of abnormalities of the autonomic nervous system and hormonal function.  As discussed in my post of 29^th June, one of the most thought provoking aspects of over-training is the possibility that it is associated free radical damage arising from the failure to re-cycle ADP.  

The high energy molecule, ATP (adenosine triphosphate), is the immediate source of the energy that drives muscle contraction.  It is a molecule consisting of a purine (adenine) and a ribose sugar molecule  linked via high energy chemical bonds to three phosphate groups.  When ATP is harnessed to drive muscle contraction, it is split to produce ADP (adenosine diphosphate) and a phosphate ion.  Most of the ADP is re-cycled in the process of regenerating ATP in the final stage of either aerobic or anaerobic metabolism.  However, a proportion of the ADP is not recycled, but instead is degraded to uric acid.  The process of degradation of ADP generates free radicals – very reactive molecules that can damage muscle tissue by oxidation.  Such damage would be expected to have long-lasting effects, and perhaps even be irreversible, especially in the older runner.

The facts regarding free radical damage remain uncertain.  There is ambiguous evidence regarding the benefits of anti-oxidant supplements.  However, after weighing-up the various strands of evidence, I am inclined to believe that for the runner who wants to continue to enjoy running into old age, one of his or her maxims should be to train as little as is necessary to achieve his or her goals.

The challenge

Thus, I am on the horns of a dilemma.  I believe that the successes of contemporary African distance runners, and perhaps even my own modest successes as a marathon runner four decades ago, were based on the cumulative benefits of many years of vigorous exercise.  Yet, there is also a body of evidence suggesting that excessive training might ultimately result in long term damage.   I am therefore going to have to make some shrewd judgments in the design of my campaign to yet again run a creditable marathon and to continue to enjoy running for many years after.

In the past few weeks I have been doing a lot of thinking about this challenge, and I have almost completed crafting my plan – a plan that will no doubt require adjustment as the years go by.  It is a plan that entails periodization.  Every period will include ‘foundation’ activities designed to promote continuous development of blood vessels supplying heart and leg muscles, and the development of the aerobic capacity of type 2A muscle fibres, as I believe that both of these adaptations are an essential foundation for engaging in moderately high intensity training without subjecting the body to remorseless stress.  Each period will also have a specific focus.  The specific focus of the first period will be improving the strength of my leg muscles. 

In my next posting I will provide an outline of the overall plan for the campaign to run a good marathon in 2012, together with a more detailed account of the plan for phase 1.

In recent weeks I have been exploring ways of training my non-conscious brain to relax its apparently over-protective control of my cardiac output.  I think I have been successful, though at the price of straining a muscle – it is very difficult to get everything right.  Nonetheless, I am sufficiently encouraged by the gains to examine the way in which similar principles might be applied to other aspects of running.  The underlying principles that I have been employing are the principles of cognitive behavior therapy (CBT).  This is a form of therapy that has been widely used in recent years for treating a range of minor mental problems; some enthusiastic advocates see it as a technique for dealing with all sorts of everyday challenges.  In reality, panaceas don’t exist, but because some of the principles mesh with the growing evidence about the role of the brain in shaping our running, it is worth a closer look

Cognitions, behaviour and childhood development

CBT is a form of psychological therapy that deals with practical problems in the here and now, and  is often regarded with distain by psychotherapists who believe that change in human emotions and behavior is best achieved by dealing with deep rooted maladjustments that have their origins in early childhood.  It is almost certainly true that childhood experience shapes both our minds and our bodies – more striking than the genetic endowment of elite African distance runners is the observation that many of them ran to and from school every day in early childhood.  As someone who also had the good fortune to run to and from school each day for several years, I suspect that the long-term benefits were not merely increased development of heart and leg muscles, but also arose from both conscious and non-conscious memories. 

There is little evidence that it is effective to try to change the consequence of childhood development by regression to childhood.  That is the tortuous path mapped out by Woody Allen in his depictions of neurotic New Yorkers dependent on weekly visits to their therapists.   In contrast, CBT is short term and problem oriented.  There is good evidence that it works for treating depression and anxiety.  Of course when testing the effectiveness of psychological treatments, it is impossible to employ a ‘gold standard’ double blind controlled trial in which neither therapist nor patient know whether the patient is getting the treatment under test, or an inert comparison (placebo).  However the evidence from fairly well controlled but non-blinded studies does show that CBT works for mood disorders, and has efficacy similar to that of antidepressant medication (see for example the review by Cuijpers and colleagues, J Clin Psychiatry. 69(11):1675-85, 2008)  

Can the same principles be used to get the best out of our non-conscious brains when we run?  The core principle of cognitive therapy is that our conscious thoughts often involve us jumping to self-defeating negative judgment about ourselves that lower our mood and paralyze our performance.  That is the C part of CBT.  Just as important in the B part.  B denotes behavior therapy.  Thirty years ago, behavior therapy alone was in vogue.  It was a way of changing behavior based on observations of the ways in which laboratory rats or dogs can be trained. 

Similarities and differences between humans and other animals

The studies of animals demonstrated two common types of learning: Pavlovian conditioning which entails learning to respond to a new stimulus by associating it with an established stimulus that has an automatic effect (eg the smell of food producing salivation); and Skinnerian conditioning: learning a new pattern of behavior as a result of rewards for small steps in the right direction.  Skinnerian conditioning works well for training rats, and in fact can also be used to train humans, but pure behavior therapy went out of fashion as a form of psychological therapy, except for young children, for two reasons.  It does not fit well with contemporary society’s belief about the importance of being in charge of decisions about ones own life.  Secondly, and perhaps more importantly, it fails to utilize one the amazing things about the human mind and brain: our ability to make conscious decisions based not only on immediate rewards, but also on memories of the past and on plans for the future.

CBT attempts to incorporate conscious evaluation, planning and decision making with the type of automatic learning processes that work well in other animals.  In principle this makes sense: all of the basic building blocks of the human brain can be found in the brains of other animals and it is therefore likely that training strategies that work for rats in the laboratory, might also work for humans.  But despite being built of the same building blocks as the rat brain, the human brain has an immensely richer network of connections between the building blocks, and the richness of these connections endows us with what we experience as the ability to make conscious decisions.  But sometimes conscious thought can get in the way.

Pacing ourselves

In the domain of running, one of the unanswered mysteries is how we pace ourselves during a race.   It can scarcely be dependent entirely on conscious memory from previous races, but neither can it be a process of pushing our bodies to the limit throughout the race.   Tim Noakes and colleagues have developed the concept of the central governor which regulates effort by anticipation that is based at least in part on non-conscious processes.  The central governor hypothesis remains a hypothesis that has generated heated debate for almost 15 years.  So far, the studies designed to provide direct support of the hypothesis have not been convincing.  For example, the claim by Ross Tucker and colleagues from Noakes’ lab in Capetown that the rate of heat storage mediates an anticipatory reduction in exercise intensity during cycling (J Physiol 574: 905–915, 2006) has been criticized by Jay and Kenny on the grounds that the method of estimating the rate of heat storage was flawed (J Appl Physiol 107: 630-631, 2009). However, failure of experiments to establish the truth of the hypothesis does not prove that the hypothesis is invalid –the complexity of the human mind and body makes it difficult to obtain convincing evidence.  Nonetheless, there are many observations about the pacing of human performance that are difficult to explain by any hypothesis other than some form of anticipatory regulation, which is at least partly non-conscious. 

My own conclusion is that the central governor theory is a good framework for developing ideas, but the ideas must be tested out against experience.  Of course, many of the ideas that emerge from speculation based on science are things that our grandmothers might have told us – but if I had listened only to my grandmother, I would have given up running long before my mid sixties.  We now know enough about how the brain and mind works to justify trying to fit our own experience into a coherent framework, even though the immense complexity of the mind and brain means that the details are speculative and predictions need to be interpreted cautiously. 

So let us start by looking at the implications of principles that underpin CBT: First is the behavioral principle what is rewarded (for example, by success) will be reinforced by non-conscious mechanisms and become a part of our behavioral repertoire.  Second is the principle that cognitive responses shape human learning, but that our automatic cognitions are often self-destructive, and need to be tested against reality.  These two principles provide the basis for understanding some of the conscious and non-conscious mechanisms by which our brains set the pace when running

Five strategies

Here are five strategies that I have learned by testing my experiences against the general principles listed above.  All of these have no doubt been advanced previously by runners and coaches, purely on the basis of what experience has taught them, but over the years I have met coaches and runners who have expressed notions counter to these ideas – so at least for me, having a theoretical framework allows me to assemble a repertoire of training strategies that provide a coherent guide but nonetheless that I take with a pinch of salt:

1) Race often: racing is the best way to demonstrate to your brain just what your heart and skeletal muscles are capable of.  The excitement of the race maximizes dopamine release in the brain, and adrenaline release elsewhere in the body.  High dopamine levels (the principal  mediator of motivation) strengthen the signals the brain sends to the muscles; high adrenaline promotes strong contraction of heart muscle and efficient distribution of blood to the muscles.  So a race that is fairly hard but not totally exhausting race can be a great way to bring yourself to a peak.  However, it is essential to provide adequate time for recovery from the short term damage to muscles that racing produces.

2) Frequently run faster than target race pace in the sharpening- up phase, either by running shorter races, interval sessions or fartlek.  This teaches your brain that you still have plenty in reserve at race pace.  On the other hand, I do not regard ‘over-distance’ sessions as especially useful from the point of view of mental preparation.  Ever since childhood I have had a deeply embedded confidence that, barring a serious muscle injury, I can last the distance in any race; so at least for me, the more challenging issue is whether or not I can sustain the target pace.   Perhaps each individual needs to identify their own mental vulnerabilities.

3) Maintain conscious focus on the present:  In the mid stages of a long race, conscious focus on the distance remaining can undermine confidence of ones ability to sustain the planned pace.  Although pace judgment in a long race requires a sophisticated calculation by the brain, it is often better to leave the micromanagement of pace to the non-conscious brain.  When you focus purely on the sensations of breathing and the rhythm of running without consciously questioning how long you can sustain this, a fast pace often feels more exhilarating than daunting.  On the other hand, insidious negative thoughts can be destructive.

4) Make the most of bad days: When you body tells you that it cannot cope with a planned training session, it is generally better to aim to sustain the intended pace or even build up to a slightly faster pace for a shorter period; or maybe do some stride-outs at target race pace, but without forcing yourself; the aim is to demonstrate that there is a bit more in the tank than your brain believes, but not to wreck yourself.

5) Use you conscious brain to keep things in perspective: do not catastrophize if you have a bad session; make a mental list of the positive features of the session; be aware that the body has immense capacity to compensate for short-term minor disruptions, such as poor sleep; suboptimal food or fluid intake; minor injury – and accept that it is OK to stop if you have a definite injury – or to pause to deal with increasing local tension in a muscle.

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.

The first question on Monday morning was whether or not the previous day’s half marathon had triggered a relapse of the fatigue of the previous few weeks.  I was delighted to find that Monday’s orthostatic test was a textbook illustration: a 9.8 bpm rise in heart rate from resting to standing , with a healthy shift from parasympathetic preponderance while resting towards a sympathetic preponderance while standing.  In the subsequent two days the orthostatic test has continued to yield similar results with orthostatic rises of around 8 bpm.  I still feel tired, but I think this is normal tiredness after pushing my legs a bit harder than my training had prepared them for.  I appear to have overcome the troublesome fatigue that had hamstrung me when I attempted to recommence training after my illness.

The second question was: how serious was the strain of my left hip adductors that had developed midway through the half-marathon?  On Monday morning there was a dull ache in my upper thigh, and I made no attempt to test the situation any further.  Tuesday evening I did a short easy session on the elliptical cross-trainer without exacerbating the problem, so this morning, I did some cautious hip swings.  I found I could swing the left leg to 90 degrees without trouble.  On the right, I could swing only to about 60 degrees without pain.  The task of preventing rotation of the pelvis when swinging the opposite leg places greater demands on the adductors of the stance leg, so this was not surprising.  I was sufficiently encouraged to try an easy run this evening.  However as soon as I started to jog, the pain returned so I stopped immediately.  The adductors need a few more days of rest, but I am hopeful I will be running again before too long. 

Although my primary goal on Sunday was to test my recovery from fatigue, it was not all about watching the heart monitor.  A few photos from the final stages give a glimpse of some of the other features of the run.

In the first picture, on the left, taken about 120 metres from the finish, I am managing to maintain reasonable form.  But with the limited swing of my right leg, a firmly anchored left foot and short stride, I certainly do not look as if I am racing.   The second photo, about 80 metres from the line, shows that despite my short stride and almost non-existent airborne phase, the gap separating me from a runner from Redhill Road Runners (7484) is closing.  The picture catches me relatively late in the swing of the left leg.  There is visible tension in my hip adductors.  At this stage of the gait cycle the main role of the hip adductors is to assist the extensors in arresting the swinging leg and bring the foot backwards relative to the torso.  On account of my feeble swing, that should not have required much muscle power.  I presume the overt tension reflects a mild spasm due to torn fibres.

However it was the next picture that brought back a bit of nostalgia for times past. In the few long races I have run since recommencing running in middle age, I have let the lingering remnants of the competitive spirit of my youth to have free rein in the final kilometer or so.  If two runners are shoulder to shoulder after 20Km, they are likely to be fairly evenly matched and it is usually the one with a bit more fire in his belly who crosses the line first.  But wisdom had dictated that Sunday’s run was not an occasion to let the competitive spirit go wild.  About 1Km from the end, a runner in the yellow vest of the Steel City Striders strode past me and I simply let him go without a challenge.  However here I was, within a few metres of the finish, and it was just too much to let this opportunity go by.   

If I half close my eyes looking at the picture I can almost imagine myself forty years ago – well maybe I would need to put on very dark glasses and well as half-closing my eyes to create that illusion – but at least it looks as if I am racing.  I did retain enough sense to avoid an all out sprint, and was content to cross the line a second or so ahead of my rival from Redhill.  I also overtook the young man to the right of the second photo (4184) and a young woman who is not in the field of view.  So although I had not intended to treat Sunday’s run as a race, it was good to have a brief reminder of times past.

I awoke a few minutes before the alarm to a perfect blue sky framed by the skylight. After several days of Indian summer that have almost allowed us to forget how miserable the second half of summer has been, it looked as if it might actually be warm for the Robin Hood marathon and half marathon today. Yesterday had been glorious for any outdoor activity apart from marathon running.  Would today be the same?  

However the weather was not really my main concern.  I was more interested to know whether or not the ‘post-illness’ fatigue that had held me back in recent weeks had really resolved.  For the previous two days, the orthostatic increase in my heart rate on standing had been 14 bpm, a marked contrast to the values in the range -1 to 2 bpm during the fatigue and associated parasympathetic over-activity, which I have suffered in recent weeks.   This morning the orthostatic rise was down to 6 bpm – a little disconcerting but probably not a significant reason for concern. 

My illness in June, and the fatigue that followed, had greatly curtailed my training and it was clear that the goal of 99 min that I had set 5 months previously was no longer feasible.  Now the major goal was to confirm that the low volume, graded intensity sessions of the previous three weeks had overcome the fatigue.  It appeared that the best way to do this was to set the goal of maintaining a heart rate in the range 134-137 for the full 13.1 miles.  A few weeks ago, pushing my heart rate much above this level for even a few minutes was crushingly difficult.

While the primary challenge was proving that my cardiovascular system could cope, I was aware that the truncation of my training had prevented me from preparing my legs for the task of racing a half-marathon.  An additional issue was the fact that I had been woken by severe leg muscle cramps several times in the past week, and after yesterday’s hot weather, I was a little concerned about the risk of cramp while running today.  Thomas’ graphic report of his calf muscle cramp in the final stages of the Dingle marathon in yesterday’s heat raised my concern a few notches higher, so before going to bed last night I had mixed myself several litres of an isotonic drink containing 1 gm of salt per litre (roughly the concentration of salt in sweat) in addition to about 80 gm/litre of sugar and some lemon squash.  I had drunk almost a litre before bed and planned to finish the remaining 1 ½ litres this morning before the race. 

By the time I had finished breakfast, sporadic clouds had appeared.  The combination of accumulating cloud cover, glimpses of sunshine, and the light north easterly breeze promised perfect weather for running, but nonetheless I was happy with my precautions and consumed the remainder of my drink as I walked along the embankment beside the river Trent to the starting area.

Because my primary goal was demonstrating that I had overcome the limitations provided by excessive parasympathetic activity, I had decided on the strategy of setting my pace according to heart rate.  In normal circumstances, the main problem with this strategy is that the excitement of the race might increase sympathetic output and lead to misleadingly high heart rate.  As I stood in the start corral, surrounded by milling, anxious athletes, in the few minutes between the cheer that accompanied the start of the wheelchair race, and hooter that would set the  marathon & half-marathon runners on their way, I noted that my pulse was 58.  I suspect that not too many other runners in the corral had a pulse below 60 at that moment.  It was clear that I did not need to worry about spurious sympathetic drive; on the contrary it looked as if my parasympathetic system was still overactive.  Nonetheless, I decided to stick to my strategy of aiming for a heart rate around 134-137. 

The hooter sounded and a mass of 12000 runners began to accumulate speed gradually as they moved towards and then over the starting mats.  No doubt each individual was in his or her own world, intent of what lay ahead, and mainly concerned at this stage to avoid being tripped-up in the melee.  However, to a distant observer, it must have appeared more like a single creature; perhaps some ponderous dragon awakening.  I had positioned myself with the 100-120 minute half-marathon group; and at first I let the human tide carry me forwards.  I reached the 1 mile marker in 7:45 with a heart rate of 135 and feeling relaxed.  Perfect.  

I could see the 105 minutes pace group leader a short distance ahead.  At first I thought that he had misjudged his pace, but then realized that he had probably crossed the starting mat about 15 seconds ahead of me.   His banner was an attractive target to focus on, but I knew that I should ignore it if it distracted me from my target heart rate.   As we ascended the steep climb to Nottingham Castle I allowed my heart rate to rise to 140, but set that as a definite upper limit.  I lost sight of the 105 minute pace leader.  Runners streamed by, many panting with the exertion of the climb.  Rounding the sharp corner beneath the Castle gate, I was delighted by the rousing rhythms of a jazz band.    

The 105 minute pace leader was again in sight and I settled back to cruise at 135-136 bpm.  In the melee of the first water station shortly after 3 miles, I again lost the 105 minute group.  By this stage I was able to select my own path on the road some of the time, but at corners or any other narrowings, we were still hemmed in like African wildebeests in a mass migration.   A short while later, after beginning the gradual ascent towards the ridge that dominates the north east corner of the university campus, I passed Mick and Phil.   Those unfamiliar with the UK running world might not be aware of this inspiring duo.   Mick pushes his severely disabled son in a wheelchair – not one of the whizzy racers but a barely modified ‘domestic’ wheelchair.  Last week they had completed the Wolverhampton marathon in 4:39, and, it appeared that they were moving somewhat faster today, though seeing Mick pushing Phil uphill with more than 22 miles still to go, one couldn’t help feeling humbled by their prodigious effort.

Again I allowed my heart rate to rise to 140 on the ascent, and was pleased that there was no sign of the crushing fatigue that I had experienced around that effort level a few weeks ago.  Then there was the helter-skelter descent to the university lake.  I thought ruefully that it was unfair to have to toil steadily uphill for about a mile and then throw away the fruit of that effort in a few hundred yards of knee-jarring descent.  However I consoled myself with the thought that the two remaining substantial hills would each be followed by a gentle down-slope.

Along the shore of the lake I was still hemmed in, but really enjoying the run.  Then came the ascent back to the ridge top.  Again I limited my heart rate to 140, and a handful of runners moved past me, though by this stage, there were others prepared to let their pace drop on the ascents.   Although I was feeling comfortable as I approached the drink station at 6 miles and the weather had remained perfect with almost continuous cloud-cover, I decided to take the offered bottle of Lucozade.  Despite the somewhat sickly sweetness of isotonic drinks while running, I thought it was best to keep my salt level topped- up.  I sipped about half of the 300ml bottle over the next half mile before abandoning it.

By this stage I was descending past the halfway point and pondering whether or not to increase the pace a little.  The 105 minute pace leader was still in sight about 100 yds ahead.  It was now 51 minutes into the race and I was sure he was going a little too fast. I was also beginning to wonder if a time not much over 100 minutes might be within reach.  But then things went seriously wrong.  I had been aware of a tightening of the hip adductors in my left leg since the sharp turn though the gates out of the University campus, and as I increased stride length approaching the 7 mile marker, the pain became quite intense.   I was unsure whether or not to continue.  My legs were clearly not adequately conditioned for a hard half-marathon, and there was a risk of significant muscle damage.  In any case, unless I could do something to relieve the rapidly increasing tightening of my adductors, I would have no option but to slow to a painful limp.

As I turned the corner towards the entrance to Wollaton Park and began the long ascent to Wollaton Hall, I shortened my stride to about 60 cm and the pain in my adductors began to ease.  Despite a cadence of over 200 steps per minute, my pace was now about 8 min/Km (or 12 min per mile).   However, by the drink station at 8.5 miles, just beyond the summit, the pain was easing and I decided to carry on.  Instead of the hoped-for powerful surge down the gentle slope though the deer park in compensation for the slog up to the Hall, I was limited to a very tentative increase in speed. The 105 min pace leader was now out of sight.

Although the adductors continued to nag me, I gradually picked up speed and after leaving the Park, just beyond the nine mile marker, I saw the 105 minute pace leader ahead again.  I decided that fate had declared that he would be my lodestar today, and set out to close the gap.  I drew up to his shoulder at 10 ½ miles but had the feeling I could cope with a faster pace, so I passed him and began steadily working my way forward through the field.  Despite the continuing nagging of my adductors I was fairly comfortable maintaining a pace of around 7:55 per mile. 

Subsequent examination of my heart rate recording confirmed that I was minimally stressed.  Here is the trace of heart rate for a three minute segment at around 80 minutes and also the Poincare plot for the 10^th and 11^th miles.  The heart rate trace shows fluctuations at a rate of about 50 peaks per minute.  As I was breathing at a rate of one breath every four steps, and my cadence was still around 200, these fluctuations almost certainly matched my breathing rate and represent a healthy sinus arrhythmia – the parasympathetic driven fluctuations that ensure that cardiac filling is greatest when the level of oxygen in the lungs is at its highest.  

Heart rate trace and Poincare plot during the 10th and 11th miles of the half-marathon

The wide spread of point across the 45 degree line in the Poincare plot confirms a strong parasympathetic drive.  The figure also shows the amount of power in the low frequency range (0.04-0.15 cycles per sec) and the high frequency range (0.15 to 0.4 cycles per sec) of the heart rate power spectrum.  The low frequency activity reflects sympathetic activity while the high frequency reflects parasympathetic activity (though it should be noted that the upper boundary of 0.4 cycles per sec agreed by an  international committee of cardiologists, is actually below the respiratory frequency when running at this pace, and therefore, the high frequency power does not include the respiratory fluctuations).  Nonetheless, there is still greater power even within the high frequency range truncated at 0.4 cycles per sec, providing strong evidence that the balance between sympathetic fight/flight and parasympathetic rest/recovery was tipped towards parasympathetic activity.  Normally one would expect an excess of sympathetic activity at this stage in a half marathon.  Overall, this data is evidence that my parasympathetic system is still being a bit over-protective, but unlike the situation a few weeks ago, I was able to maintain my heart rate near the intended level, without any feeling of fatigue. 

My main problem was my nagging adductor muscles.  As I had stepped-up the pace, the pain had increased again, so I eased back a little in the final mile or so to minimize damage, and crossed the finish line in 103:28 (chip time 103:17).  My average heart rate for the entire race was 137 bpm.  Ninety-two seconds later, the 105 minute pace leader crossed the line, on schedule to within a second.    

I sit here now with a painful thigh, unsure how much damage I have done, though I do not think it is very severe.  A time of 103:28 for a half marathon is not in itself a great achievement.  If my goal had been a fast time, it would have been foolish to have continued beyond the 7 mile point.   However, this summer various circumstances have conspired against me, and I had been forced to set aside the target time selected five months ago.  Although I had been undecided about starting the race until about two days ago, once it was clear that my fatigue was resolving, running the event with the target of maintaining a heart rate of 134-137 became as important a goal as running a half-marathon in 99 minutes had appeared to be in May.  It was potentially a stringent test of whether or not I have overcome the fatigue.   In the event, I achieved my target despite the adductor problem. 

It was especially pleasing to have been within 4 ½ minutes of my original target time despite seriously curtailed training.  It is tempting to think I might have even achieved the 99 minute target today if it had not been for the injured adductor, but this is very improbable.  The primary problem was that my legs had not been conditioned by an adequate number of tempo and long runs.  Although the overt limitation was provided by the adductors, in fact my legs could not have coped with a much faster pace.  Both legs felt like jelly afterwards, and I was wobbly on my feet for a few hours, quite apart from the limp.  My legs could not have carried me much faster, but it is encouraging to know that my heart appears to have coped well.

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 not running for several days, I decided that tonight I would do a short run of about 5Km, including a few stride-outs.  By the time I got home from work it was around 8pm, almost dark, and the rain was pelting down.  However once I had my trainers on, I was eager to go.

The chilly gust of wind that greeted me as I opened the door sent me back inside to put on a long sleeved top – undoubtedly summer has ended.   Because the last glimmer of daylight was fading rapidly, I decided to run on the sidewalk rather than my usual path along the river bank.  After a short distance I passed a young woman jogger who was dressed or perhaps more accurately, un-dressed, for mid-summer, with a large expanse of bare mid-riff between her skimpy top and shorts. As the wind whipped the rain against my face I was quite glad I had gone back for a long sleeved top, even though it was already quite soggy.

During the stride-outs over a distance of 200-300 metres at a pace of around 4:45 per Km, I managed to remain fairly relaxed, though to have run any faster would have been quite effortful.  Afterwards I thought ruefully that 4:45 was a little slower the pace I had originally intended for the half-marathon next week.  That goal is now unthinkable, but I at present I am happy that the fatigue of the past few weeks seems to be gradually receding and I am still running.