Archive for the ‘Training’ Category

The big debates of the past decade: 3) High intensity v high volume training

March 31, 2014

The debate between high intensity and high volume training has been a perennial topic since the early days of scientifically-grounded training.   Interval training was developed in the 1930’s by the German coach and academic, Woldemar Gerschler. He based his recommendations on the theory that the heart muscle would be strengthened by the increase in cardiac stroke volume that occurs as heart rate drops immediately following an intense effort. A decade later, Gerschler’s compatriot, sports physician Ernst van Aaken proposed that the crucial requirement was delivering copious amounts of oxygen to the heart, and this could best be achieved by running long distances at relatively slow paces. It is noteworthy that a large volume of slow running also increases delivery of oxygen to the leg muscles. Van Aaken’s approach was later developed by New Zealander, Arthur Lydiard, based largely on trial-and-error adjustments of his own training. Lydiard’s method led to medals for his athletes, Peter Snell, Murray Halberg and Barry Magee in distances from 800m to the marathon at the Rome Olympics in 1960. While Lydiard promoted a high volume approach to building basic aerobic fitness, his program also included periodization – a progression from base building to a period of race specific training and final sharpening immediately prior to competition.

Meanwhile, interval training retained its devotees and underpinned the golden age of British middle distance running that reached its pinnacle with Seb Coe’s Olympic gold medals in the 1500m in 1980 and 1984.   By the end of the century, Japanese academic, Izumi Tabata had demonstrated that repeated very intense brief maximal efforts lasting only 20 seconds separated by even briefer recovery periods, produced impressive increases in aerobic capacity (reflected in increases in VO2max) while also enhancing anaerobic capability.

Meanwhile, devotees of high volume, less intense training, led by charismatic individuals such as John Hadd and Phil Maffetone, emphasized the risk that focussing on high intensity training might undermine sound long term development.   So what has the past decade contributed to this long-standing debate?

I think that three main strands of evidence have advanced the debate. These strands are: evidence from physiological investigations; the training of African distance runners; and evidence from a small number of fairly well conducted controlled comparisons of different training protocols

Physiological investigations

The fundamental principle of training is that training produces stress on the various physiological systems within the body, such as the cardiovascular system, skeletal muscles and the nervous system, and subsequent adaptive change as the body responds to that stress leads to increased fitness. The past decade has seen an explosion of knowledge about the multitude of biochemical signalling processes that trigger these adaptive changes. In addition to the hormones produced by the major endocrine glands, there are a vast number of other relevant signalling molecules, including the numerous cytokines that regulate inflammation (the cardinal process that mobilises repair in tissues throughout the body) and growth factors that promote changes in many tissues. In particular, growth factors and hormones promote the activation of satellite cells in muscle. These satellite cells are a type of stem cell that fuse with muscle cells to repair and strengthen them.

While this explosion of knowledge does provide useful clues regarding the way the body might react to various forms of training, at present the complexity of the information precludes any simple answer to the high volume v high intensity debate. It does however provide support to both sides, indicating that the best answer will prove to be a combination of the two.

In light of concerns that high intensity training might destroy the aerobic enzymes that catalyse the chemical transformations involved in aerobic metabolism in the mitochondria of muscle cells, it is of particular relevant to note that a series of studies, Gibala and colleagues at McMaster University in Canada have demonstrated that high intensity interval training is as effective as high volume training for developing these aerobic enzymes. Furthermore, Bangsbo and colleagues in Copenhagen reported that speed endurance training consisting of six to twelve 30 second sprints 3-4 times/week for 6 – 9 weeks improved ability to pump the potassium ions back into muscle cells. Potassium ions are expelled from muscle during exercise. The depletion of potassium within the muscle probably plays an important role in fatigue.   Bangsbo demonstrated that the improved ability to pump potassium back into muscle cells was accompanied by an average improvement of 18 seconds in 3 Km race time, and an average improvement of 60 seconds in 10 Km time, in a group of 17 moderately trained male endurance runners


Elite Africans

The most striking feature of elite distance running in the past decade has been the dominance of African runners, mainly from the highlands of Kenya and Ethiopia. There have been many anecdotal accounts that make it clear that high volume training, with several training sessions per day, is an important aspect of the training program of virtually all elite Africans. Usually the day’s program includes one session of quite low intensity running, but many accounts also describe other sessions of quite intense running – especially sustained tempo efforts.  I will not attempt to review all this information here, in part because of its diversity but even more importantly, it remains unclear just how much cultural factors (such as running to school in childhood); multiple genetic factors; and up-bringing at high altitude have contributed to the African dominance.   It remains to be demonstrated convincingly that the training methods employed in Africa can adapted to produce similarly impressive performances by non-Africans.

I will nonetheless draw attention specifically to the training methods adopted by Renato Canova, coach to many of the leading African half-marathoners and marathoners. I have described Canova’s training previously. In his lectures and writing, Canova places little emphasis on low intensity running, perhaps because the athletes he trains have already achieved extensive development of capillaries and other aspects of type 1 fibre development. Nonetheless, the training dairies of the athletes he coaches reveal that in addition to the relatively intense sessions there is a large amount of low intensity running. For example about 80% of the training of Moses Mosop is at an easy pace, with occasional sessions as slow as 5 min/Km (which should be compared with his marathon pace of around 3 min/Km). Canova advocates a periodized approach. The crucial feature of the race specific phase is long runs at near race pace.

Controlled comparisons of training programs

As mentioned above, some of the studies comparing high intensity interval training with standard endurance training, such as the study by Bangsbo and colleagues, demonstrate greater improvement in performances over distances from 3Km to 10Km with the high intensity training, while others, such as those by Gibala and colleagues report similar gains in performance with high intensity training and conventional endurance training, although the high intensity programs achieved similar benefit from a much smaller volume of training. However, those studies were performed over a time scale of approximately 8 weeks. This is scarcely long enough to exclude the possibility that high intensity training might result in a harmful accumulation of stress.

The question of longer term effects was tested in a study by Esteve-Laneo and colleagues from Spain.  They randomly allocated 12 sub-elite distance runners to one of two training programs: a polarised program involving a large amount of low intensity training and small volume of moderate and high intensity training; and a threshold program involving a predominance of training near lactate threshold and a small amount of higher intensity training, for a period of five months. Training was classified in three zones: low intensity below the first ventilatory threshold (VT1) corresponding to the point where lactate rises to around 2 mM/litre; moderate intensity between VT1 and the second ventilatory threshold (VT2) corresponding to the point where lactate exceeds 4 mM/litre; and high intensity, above VT2 during which lactate accumulates rapidly. In the polarised program the proportions of low-, moderate- and high-intensity training were 82%, 10% and 8% while the proportions in the threshold program were 67%, 25% and 8%. At the end of the program, the group allocated to polarised training achieved significantly better performances in a 10.4Km cross country race.

More recently, Stoggl and Sterlich from Austria performed a study comparing a 9 week polarised training program with three other programs: high intensity; high volume (low intensity) and predominantly tempo training, in a sample of national class endurance runners, triathletes, cyclists, and nordic skiiers. The polarized training group exhibited the greatest improvement in VO2 max (+ 11.7%) and time to exhaustion (+17.4%). The high intensity group achieved a 4.8% increase in VO2 max and an 8.8% time to exhaustion 8.8 percent.  The high intensity group lost 3.8% of body weight, which Stoggl and Sterlich attributed to a harmful catabolic state. Improvements were small and insignificant for the other two training programs. It should be noted that these athletes were a national standard and had probably achieved the improvement that might be expected from either a high volume of low intensity training or from a predominance of tempo training.

Neal and colleagues used a cross-over study design in which a group of well-trained cyclists underwent polarised training and threshold training, each for 6 weeks in randomised order. Similar baseline fitness was established by a 4 week de-training period before each training period. The proportion of training time in low-, moderate and high intensity zones was 80%, 0%, 20% in the polarised program, and 57%, 43% and 0% in the threshold program.The polarised training produced greater increases in peak power output, lactate threshold and high-intensity exercise capacity (time to exhaustion at 95% maximum work rate).


Summary and Conclusions

Stephen Seiler, a Texan sports scientist based in Norway for the past decade, presented a summary of the evidence from the controlled comparisons of different training programs and also from studies that have examined the proportions of training time that elite athletes spend in different intensity zones, at a lecture delivered in Paris in October 2013. He provided a compelling argument for polarised training. However, despite the evidence that many elites follow a polarised program, the role of key sessions at a pace near to race pace in the training recommended by Renato Canova indicates that at least a modest proportion of threshold training is beneficial for marathoners. Furthermore, Canova recommends a moderate degree of periodization with a clearly defined period of specific preparation for key races.

Overall, it is likely that any sensible training program will produce benefit for an unfit athlete provided it is consistent. However for an athlete who has achieved a plateau of fitness, it is probable that a polarised program with proportions of low-, moderate- and high-intensity of approximately 80%, 10%, 10% is most effective. Nonetheless, during a period of preparation for a specific race the key sessions should incorporate running at a pace near to race pace.

The five big debates of the past 10 years

February 6, 2014

The past decade has seen a continued growth of distance running as a mass participation sport.   The major city marathons continue to attract many thousands of entrants with aspirations ranging from sub 2:30 to simply completing the distance in whatever time it takes.  Perhaps more dramatically, parkrun has grown from a local weekly gathering of a few club runners in south-west London to an event that attracts many tens of thousands of individuals at hundreds of local parks, not only in the UK but world-wide, on Saturday mornings to run 5Km in times ranging from 15 min to 45 min before getting on with their usual weekend activities. Over this same period, the ubiquity of internet communication has allowed the exchange of ideas about running in a manner unimaginable in the days when distance running was a minority sport pursued by small numbers of wiry, tough-minded individuals whose main access to training lore was word- of-mouth communication.

Not surprisingly, within this hugely expanded and diverse but inter-connected community there have been lively debates about many aspects of running, with diverse gurus proposing answers to the challenges of avoiding injury and getting fit enough to achieve one’s goals.   Pendulums have swung wildly between extremes.  My impression is that the fire in most of the debates has lost much of its heat as the claims of gurus have been scrutinised in the light of evidence.   However, definitive answers have remained elusive.   What have we learned that us useful from this turbulent ten years?

There have been 5 major topics of debate:

1) Does running style matter and if so, is there a style that minimises risk of injury while maximising efficiency?

2) Are minimalist running shoes preferable to the heavily engineered shoes promoted by the major companies?

3) What is the optimal balance between high volume and high intensity training in producing fitness for distance running?

4) Is a paleo-diet preferable to a high carbohydrate diet?

5) Does a large amount of distance running actually damage health, and in particular, does it increase the risk of heart disease.

In all five topics, debate still simmers.  I have scrutinised the scientific evidence related to all five of these question in my blog over the past seven years, and I hope I will still be examining interesting fresh evidence for many years to come.   However whatever answers might emerge from future science, in our quest to determine the answers that will help us reach out running goals we are each an experiment of one and now is the point in time when we must act. I think that the evidence that has emerged in the past decade has allowed me to make better-informed choices in all five of these areas of debate than would have been possible ten years ago.   In my next few posts, I will summarise what I consider to be the clear conclusions for the past decade of debate, what issue remain uncertain, and what decisions I have made with regard to my own training and racing.

For me personally, the greatest challenge as I approach my eighth decade is minimising the rate of inexorable deterioration of muscle power, cardiac output and neuro-muscular coordination that age brings.  Therefore my approach to these debates is coloured by the added complications of aging.  Nonetheless, my goal is not only to continue to run for as many  years as possible, but also to perform at the highest level my aging body will allow during these years.  I hope that the conclusions I have reached will be of interest to any runner aiming in to achieve their best possible performance, whatever their age.

Why do marathon runner slow down – the role of muscle damage

January 5, 2014

While planning the next few months of base-building for a marathon in the autumn, I have been pondering the question of what are the most important foundations for marathon running.   The marathon is run in the upper reaches of the aerobic zone, so at first sight, the most important goal of training is extending the duration for which one can maintain a pace in the vicinity of lactate threshold.   This requires a good capacity for metabolizing lactate, so developing that capacity will be part of my base-building.

Perhaps the most infamous feature of the marathon, at least in the mind of many recreational runners is the ‘wall’ that awaits somewhere near the 20 mile mark.   It is often assumed that this wall reflects the point at which glycogen stores are exhausted, and all available glucose is shunted away from muscle to the brain.  For the ill-prepared runner, that might well be a major issue, but dealing with the risk of serious glucose depletion should be relatively straightforward.   A large volume of low to mid-aerobic running and sensible nutrition in the preceding months should ensure that a good proportion of the fuel at marathon pace is derived from fat, thereby conserving glycogen, which together with adequate ingestion of carbohydrates during the race itself, should minimise the risk of a shortage of glucose.

While it is true that for many marathoners the gruelling memories are centred on the final few miles, in my own memories of the times when I have run a marathon with inadequate preparation, the  point at which I became aware that I was not running well occurred shortly after half-way.   At that stage, the problem wasn’t breathlessness, or agony.  It was a loss of fluency in my stride.   I was therefore intrigued by Reid Coolsaet’s account of his tribulations in Fukuoka in December.   Reid’s blog provides the best personal account of elite marathoning available on the web.

Reid Coolsaet in Fukuoka, 2013

Reid had arrived in Fukuoka better prepared than ever and was aiming for sub 2:10; a PB and a Canadian national record.  He started in the leading pack behind the pacemakers, Collis Birmingham and Ben St. Lawrence from Australia, running 3 min Kms (2:07 pace).  When the lead pack split on an upward slope just before 16Km Reid sensibly opted to stay back with the second group, which included one of the current leading Japanese marathoners, Arata Fujiwara, who has a PB of 2:07.  However Fujiwara was having a bad day and the second group slowed too much so Reid left them at 18Km and ran on alone.   He was still comfortable maintaining his target pace when he reached half-way in 1:04:11.  He then lost a few seconds as a consequence of grabbing the wrong bottle at the 25.8Km water station.  He covered the 5Km from 30 to 35 Km in 15:51 but was not too worried at that stage. He reports that after 35km the going got really tough and he began to ‘lose it mentally’.  He eventually finished in 6th place in a very creditable 2:11:24, just over 5 minutes behind the winner, Martin Mathathi of Kenya.

Reid had again demonstrated that he is not very far behind the best of the current North American marathoners, despite lacking the resources of Nike’s Oregon Project.   In his own analysis, the problem was running solo from 18Km to the end.  That was almost certainly part of the problem.  However, despite the seconds lost as a result of the confusion with the wrong bottle at 25.8Km, I think that the crucial evidence that the wheels were coming off was the 15:51 split from 30 to 35 Km. I suspect that the damage had been done in the first 15 Km, which he had covered about 1 minute too quickly.   But what was the damage he had done?   I doubt that the burning a little more glucose in the first 15 Km nor the confusion with his re-fuelling had left him in a glycogen depleted state by 30Km.

Running pace decrease and markers of muscle damage during a marathon

I think perhaps a clue is to be found in the recently published study of marathon runners by Juan Del Coso and colleagues from Madrid.  Del Coso performed a variety of physiological measurements on a group of 40 amateur runners immediately before and after the 2012 Madrid Marathon.  The investigators retrospectively divided the runner into two groups according to how well they maintained pace during the race.  The group of 22 runners who exhibited a decrease in pace of less than 15% from the first 5Km to the end were classified as having maintained their speed, while the group of 18 runners who slowed by more than 15% between the first 5Km and the end were classified as having a pronounced decrease in speed.  The decreased speed group slowed their pace by an average of 29% while the group classified as having maintained speed exhibited an average decrease of 5%.

The most interesting feature of the 5Km split times over the course of the race was the fact that the group with a pronounced pace decrease began to slow-down  markedly shortly after half way.  The difference in pace between the two groups became statistical significant for the split from 20 to 25 Km.  But even more interestingly, the most significant difference in the physiological measurements was a much greater increase in the blood levels of the muscle proteins, myoglobin and lactate dehydrogenase, between the start and finish in the group who slowed.  These proteins are markers of muscle damage.    Both group exhibited a decrease in counter move jump (CMJ) height from before to after the event, but this decrease was greater in the group who slowed substantially.  The group who maintained their speed exhibited a 23% decrease in CMJ height, while the group with pronounced slowing suffered a 30% decrease.

Both groups of runners exhibited a decrease in weight of approximately 3%, assumed due to dehydration.   There was no evidence of decrease in blood glucose in either group.  The runners had been allowed to take fluids and carbohydrates according to their own inclination during the race.  There was no appreciable group difference in body temperature.  Thus, there was no evidence that dehydration, decrease in blood glucose, or hyperthermia, accounted for the different degree of slowing of the groups.  It is also noteworthy that there had been no significant difference in prior training volume between the groups. In fact the group who showed the most pronounced slowing has actually performed a slightly larger volume of training.

Thus the findings from this study suggest that for reasonably well- trained amateur runners who are allowed to re-hydrate and re-fuel according to their own inclination during the race, the major feature that is associated with deteriorating pace is muscle damage.  Furthermore the deterioration becomes manifest shortly after the half-way point.

The observation of appreciable loss of strength and power, together with increased levels of muscle proteins in blood indicating skeletal muscle damage during endurance events, has been reported previously.  For example, the year previously Del Coso and colleagues had studied 25 triathletes participating in a half-ironman event.  They found that after the event, the capacity of leg muscles to produce force was markedly diminished while arm muscle force output remained unaffected.  Leg muscle fatigue was correlated with increases in blood levels of the muscle proteins, myoglobin and creatinine kinase, suggesting that muscle breakdown is one of the most relevant sources of muscle fatigue during a half-ironman.

My own experience

Looking back to my own experience in the half marathon in September, I was aware of aching legs though much of the race. Indeed I had been experiencing pronounced aching of the legs following most of my long runs during the preceding months.  In my recent post I had discussed the possible role of elevated cortisol in my mediocre half marathon performance.  While a link between cortisol and muscle damage is speculative, it is perhaps plausible that sustained elevation of cortisol had left me in a catabolic state with reduced capacity to repair muscle damage following long runs, for a period of several months.

What are the implications for base-building this year?  The first implication is that I should build up the length of long runs cautiously to minimise the risk of developing a catabolic state. I am even considering adopting Geoff Galloway’ s run/walk approach to see if I can build-up to a weekly training volume of 50 miles or more without persistent aching of my legs.   A far as I can see there has been little good independent scientific investigation of the run-walk strategy though I think there are reasons to think that it might be a sound approach – and not just for elderly runners such as myself.   I will discuss this in a future post.

An alternative approach is to include more sprint training.   In a study of the muscle damage produced by drop-jumping (which is often regarded a good model f the eccentric stress produced by running, Skurvydas and colleagues compared sprinters with long-distance runners and a group of untrained controls.  Following 100 maximal effort drop-jumps, the sprinters experienced a smaller reduction in counter-movement jump height than the other two groups, while there was no appreciable difference in evidence of damage suffered by the distance runners and the untrained controls.  It appears that sprint training might protect against muscle damage much more effectively that long-distance training.

Re-appraisal: the benefits and damage produced by cortisol

December 30, 2013

This year has been frustrating in an undramatic but challenging way.  Undramatic because I have remained free of overt injury apart from some persistent though relatively mild problems with my joints and ligaments, but challenging because it has not been easy to identify why my fitness improved so slowly and then degenerated so rapidly.  I achieved a greater volume of training –  approximately 2000 miles (including the mileage equivalent of my elliptical cross-training sessions estimated on the basis of 100Kcal = 1 mile)  than in any year in the past four decades.  Taking account of my slower training paces, it is probable that I have actually spent more time training this year than during any year in my entire life.  Yet through the summer I was frustrated by the tardy rate of improvement in fitness.

There were few occasions when I experienced the exhilaration of running fluently and powerfully.  I felt tired much of the time and experienced persistent aching of the connective tissues in my legs.  My short term goal was a half marathon time faster than 101:50.  Despite the fact that I was unable maintain a pace of 5 min /Km (corresponding to 105:30 for the HM) for even a few Km as the date of the event approached, I nurtured the hope that a three week taper with some drills and faster running to sharpen my pace, would allow me to defy any rational prediction based the evidence of my limited fitness.  However, in the event, rational prediction was indeed confirmed and despite a spirited finish, I recorded a time of 107:45.

In the aftermath I took some consolation from the fact that I had coped with a large volume of training without injury, though I was aware that I would need a few easy months to allow my body to recover.  I cut my training volume to an average of slightly less than 30 (equivalent) miles per week, including an increased proportion of elliptical cross-training.   After a month or so, I added a modest plyometric program as described in my previous post.   The encouraging outcome was a modest improvement in hopping and jumping, indicating some gain in musculo-tendonous resilience and eccentric strength, but the dominating feature of the final few months of the year has been a devastating loss of fitness.     Although I had cut my training volume substantially, the cut was less ruthless than the cut forced upon me by an episode of arthritis a year ago, yet the loss of fitness has been far greater.  I am now at my lowest ebb since summer 2011 when a hectic and exhausting six months at work had left me with neither the time nor energy for solid training.  In 2011, my lack of fitness illustrated the fact that for the elderly, fitness is hard won and easily lost.  But in 2013, I am facing the disconcerting question:  has fitness  become even more difficult to gain and easier to lose as I have moved from my mid to late 60’s, or did I do something wrong this year?

I had used submaximal tests throughout the summer to ensure that I was just one step short of over-training, as indicated by autonomic measures of stress, such as heart rate at submaximal effort and resting heart rate variability.  However, perhaps I should have taken more notice of the chronic tiredness and aching legs.    I suspect that my mediocre half marathon performance demonstrated that I was not merely over-reaching but that a least a mild degree of over-training had interfered with my ability to benefit from training.   This lurking suspicion has been strongly re-enforced by the devastating loss of fitness since September.  It is clear that I had not built a sound base.

In the past few months, I have continually questioned whether or not I simply needed a bit more rest, but on the occasions when I have cut back the training volume even more drastically for a few weeks, the deterioration in fitness has accelerated.   So the evidence suggests that I was not merely in a state of functional over-reaching from which the body bounces back with renewed vigour after a brief respite.  I had almost certainly over-trained. I was in need of a more profound rest.  Yesterday, I ran 11 Km, the longest distance I have run in recent times.  My pace was very slow – around 6:30 min/Km – but for the first time since September, my legs did not ache.  I hope this indicates that I have now passed the nadir, and can again begin re-building, but very cautiously.

Do miles make champions?

Arthur Lydiard’s simple dictum, ‘miles make champions’ is undoubtedly true.  Indeed the rapid crumbling of my fragile fitness base as I have cut back the training volume since September confirms the crucial role of training volume.  But just as every wise proverb can be countered by one that draws the opposite conclusion, miles can also undo would-be champions.   In the summer, the most striking contrast with my training of recent years was the much greater proportion of long runs, mainly at a quite slow pace.  I think it is likely that I did too many long runs this year.   As I discussed in a post in October, Dudley’s studies of rats who ran at various intensities for various durations, showed that the increase in the mitochondrial enzymes that are essential for aerobic metabolism reaches a plateau after a sufficiently long duration of running. The plateau was achieved late, and was highest, in the rats that ran at the modest pace of 30 metres/min which they could maintain comfortably for over 90 minutes.  A somewhat faster pace of  40 m/min, which was near to the peak pace that they could maintain for 90 minutes, produced a slightly lesser gain in aerobic enzymes.   Paces below 30 m/min achieved an even lower plateau. On the other hand, at paces faster 40 m/ min the gains in fitness were more rapid but the duration for which the animals could sustain the pace was less and consequently the total gain in fitness was less than that achieved at 30 m/min.

Rats differ from humans in many respects, and the actual paces of animals with legs of only a few centimetres in length are of little relevance to humans, but the muscle physiology of rats is essentially similar to ours. It is likely that similar principles govern the effects of training.  There appear to be two major conclusions.  First, the greatest gain in aerobic capacity is achieved by a ’good aerobic pace’ that can be maintained comfortably for 90 minutes.  Second, there is a limit to the benefit in aerobic capacity obtainable by increasing the length of training sessions.   There may be other benefits of long runs, such as strengthening of connective tissues. But the occurrence of the plateau in development of aerobic enzymes suggests that at that beyond around 90 minutes something inhibits the further development of aerobic enzymes.  Perhaps the most plausible limiting factor is the accumulation of cortisol.

Skoluda and colleagues have demonstrated that endurance athletes exhibit a sustained elevation of cortisol, and furthermore, the magnitude of the increase correlates with greater training volume, measured in either hours per week or distance per week.   Cortisol is a catabolic hormone that promotes the breakdown of body tissues, including muscle, while inhibiting the synthesis of new protein.    To evaluate the plausibility of the proposal that cortisol limited the synthesis of aerobic enzymes in Dudley’s rats and also played a part in my mediocre half marathon and the subsequent crumbling of my aerobic base, it is necessary to re-examine some of the details of role of hormones in the regulation of energy metabolism discussed in the first of my posts comparing the Paleo diet with a high carbohydrate diet.


At the commencement of exercise, there is an acute elevation of cortisol, together with adrenaline, that mobilizes the body’s resources to meet the demand for increased energy.   The generation of  glucose from glycogen is stimulated, thereby releasing the fuel that can be utilized most rapidly for muscle contraction.  Cortisol also stimulates the metabolism of fats and of amino acids.   Conversely, protein synthesis from amino acids slows down and body systems that serve longer term survival needs are put on hold.    The immune system and the gut suffer first, though as long as the muscle continues to generate the amino acid glutamine, which helps sustain both immune cells and the lining of the gut, these body systems continue to function reasonably well.   However, as the duration of exercise extends into the period when glycogen stores show signs of depletion, cortisol level rises further.   Now the body’s priority is ensuring adequate supply of glucose for the brain.  The increased level of cortisol inhibits the glut 4 carrier proteins that transport glucose into muscles.    The muscles are increasingly reliant on the relatively slow production of energy via fat metabolism.  Meanwhile, synthesis of glutamine drains the pool of intermediate metabolites that participate in the Krebs cycle, the closed-loop of metabolic transformations that plays a central role in energy metabolism and also in the synthesis of amino acids.  Although fat metabolism can keep the Kreb’s cycle going, it cannot top-up the pool of intermediate metabolites.  This topping-up requires input from pyruvate which is generated by the metabolism of glucose.  In the absence of concurrent glucose metabolism, glutamine levels begin to fall, impairing the function of both the immune system and the gut.

Thus, the immediate effect of the elevation of cortisol is the provision of fuel for exercise, but as glycogen supplies diminish the priority is provisioning the brain, and the rest of the body suffers.  How long does it take for this to occur?   Cook and colleagues recorded salivary cortisol levels in recreational runners both during and after a marathon. The highest level was almost 6 times higher than typical morning levels, recorded 30 minutes after completion of the event, but the level had risen steadily throughout and was already very high by 25 miles.  Similar levels were recorded following a non-competitive marathon.  Thus, an appreciable elevation of cortisol is likely even during long training runs, consistent with Skoluda’s finding that endurance athletes have chronic  elevation of cortisol that rises in proportion to training volume.

What are the potential adverse medium and long term consequences?  The acute anti-inflammatory effect of cortisol is likely to hinder the repair and strengthening of muscles and other body tissues.  In particular, the synthesis of aerobic enzymes is inhibited.  Suppression of immune function creates the risk of infections.  Sustained elevation of cortisol will sustain a balance that favours breakdown rather than building up of tissues, and thereby promote further loss of fitness.  Furthermore, prolonged exposure to high levels of cortisol decreases the sensitively of the receptor molecules that mediate the effects of cortisol on body tissues, and might ultimately promote chronic  inflammation, harming joints and connective tissues while promoting the deposition of atheroma in blood vessels.

In my own situation, I suspect that a continuing bias towards catabolism rather than anabolism has hastened my loss of fitness, while the continued aches in my legs probably reflected chronic inflammation in the ligaments.  On the other hand, I have been pleased to note that I have not suffered any exacerbation of asthma this year.  I hope that any tendency towards increased formation of atheroma in my blood vessels has been minor.

Next year, I plan to train for a marathon.  But if I am to achieve a more robust fitness base and even more importantly,  to enhance rather than harm my long term health, I need to adopt a different training strategy.   I should start with a more careful scrutiny of the past year.

Closer scrutiny of the training log

While the most immediately apparent feature of my training during summer of 2013 was the relatively high proportion of long runs, a more careful inspection of my training log reveals a potentially more significant issue.   After the resolution of arthritis in the early months of the year I had gradually increased my training volume up to 30 (equivalent) miles per week, and was coping well.  Then, in March I increased the volume quite rapidly, by almost 15%  each week for 4 weeks, up to 50 (equivalent) miles per week by early April.  The submaximal test revealed that my fitness continued to improve fairly steadily until mid-April, but then suffered a slight decline in May, so I reduced the weekly volume back to 45 (equivalent) miles per week.  Once again fitness began to improve, albeit slowly and I was feeling tired much of the time.  I continued at that level of training until mid-August when I once again increased to 50 (equivalent) miles per week, but that produced only a marginal further increase in fitness by late September.   At the time, it appeared that I had pushed myself to the limit but had not quite over-stepped the mark.  However, in retrospect, I think I had overdone it.  The damage was probably done in March and early April when I had increased training volume by 15% per week. At that time, all had appeared well, as my fitness continued to improve. Indeed from mid-March to mid-April I saw the greatest gain in fitness in any month of the year.  It appeared I had got away with a relatively minor infringement of the 10% rule.  But the increases in weekly volume reflected another feature, an increase in the number of long runs.  By late April, I was occasionally slipping in two moderately long runs within a single week.  I suspect I was accumulating a surfeit of cortisol that led to the transient decline of fitness in May, the mediocre half marathon in September and  the subsequent devastating loss of fitness.

Plans for the future

I have about nine months until my target marathon next autumn.   This gives me five months to build a solid base, leaving four months for specific marathon preparation. The cardinal goal of the final four months will be developing the capacity to sustain marathon pace for 26.2 miles.  The goals of the preceding five months of base-building  are more varied.

First, I need to ensure that my connective tissues are well conditioned and free of any trace of lingering inflammation.   I will need to adjust my training over the next few months according to how well the recent recovery is maintained.  I will continue with moderately demanding weight sessions and some mild plyometrics.  It is likely that I will do a greater proportion of my aerobic training on the elliptical cross trainer next year, and I will build-up the long runs very gradually, aiming to increase from the current 11 Km to 25 Km by late spring.

Secondly I aim to develop the ability to utilise fat in preference to carbohydrate at low and mid-aerobic paces, thereby minimising the risk of excessive elevation cortisol during long training runs.  The main element of the strategy to achieve this goal will be a gradual increase in training volume, especially in the low and mid-aerobic zones.    I will also maintain my current nutrition, consuming a diet that matches the Mediterranean diet as described in my post two weeks ago.

My third goal will be the development of aerobic capacity, including the ability to utilise lactate.  The gradual increase of training volume in the low and mid-aerobic zones required to promote utilization of fat will also contribute to this goal.  In addition, I will do regular sessions similar to Hadd’s 25×200/200 sessions, in which brief epochs that are effortful enough to generate a modest amount of lactate, alternate with recovery periods long enough to allow the metabolism of the lactate.  Because there is minimal accumulation of acidity the session is only moderately stressful.

Fourthly, I will attempt to build up the strength to maintain a reasonable marathon pace without the need to increase cadence to an inefficient level.  At present, my cadence exceeds 200 steps per minute even at 5 min/Km.  My strategy for developing the strength required to lengthen my stride includes a mixture of short hills, long hills and sprinting in addition to weights and plyometrics.  A key feature of all of these sessions will be generous recovery after each effortful epoch, to maximise the stimulation of anabolic hormones and minimise cortisol production.

Above all these specific goals, I will aim to start the marathon specific training in a robust and relaxed state.

Plyometrics and running efficiency

December 21, 2013

For several years I have been concerned about the loss of length of my stride that had become increasing marked since my early sixties.  At peak sprinting speed, my step length is less than 1 metre.  To achieve even a modest pace of 5 min/Km,  I am forced to increase cadence to over 200 steps/min.  At paces in the vicinity of 5 min/Km, efficiency tends to increase as cadence increases from 180 to 200 steps per minute because the energy consumed in getting airborne and overcoming braking decreases as cadence increases up to 200 steps /min (as demonstrated  my post of 6th Feb 2012).  However, the energy cost of repositioning the legs during the swing phase increases with increasing cadence, as discussed  in my post of 27th Feb 2012, and in my calculations performed on 5th April 2012.  Therefore, at paces in the range 4 to 5 min/Km, efficiency falls as cadence increases substantially above 200 steps per min.

Initially I considered that loss of leg muscle strength was the cause of my short stride. So a year ago I embarked on a program of weight training, mainly employing squats and deadlifts.  I was delighted that I was able to recover my lost strength, but unfortunately, it made little difference to my stride length.  I had intended to follow the initial weight sessions with some plyometrics, in the expectation that plyometrics would help me harness the increased strength and allow me to capture more elastic energy to drive powerfully off stance, but a minor relapse of arthritis confounded my plan.  By the time the arthritis had settled it was time to direct my energy towards re-building aerobic fitness for the Robin Hood half marathon in September.  I increased weekly training volume fairly rapidly but only managed a rather mediocre half marathon.

After recovering from the half-marathon, it was time re-consider my former plan to introduce plyometrics.  However, I was a little alarmed by continuous aching in my legs, especially at the attachment of peroneus  longus to the upper part of the fibula in both legs.  In addition there was a generalised aching of the connective tissues around and below both knees.  This had built up gradually during the summer and did not resolve even after I cut back the amount of training quite drastically.  By late October I was reluctant to put off the plyometrics any longer, though it was clear that I would need to be fairly cautious.

What intensity of plyometrics is required?

What evidence is there that a modest program of plyometrics would lead to a worthwhile gain in running efficiency?  A study by Turner and colleagues had assessed the change in running efficiency produced by 6 weeks of fairly gentle plyometrics in a group of moderately trained, young adult runners. The program involved adding three plyometric session per week to the runners’ usual training.  Each plyometric session involved six exercises starting with sub-maximal double-leg vertical jumps at 50% effort as a warm-up, and then proceeding to various forms of double-leg and single-leg jumps.  For example, one of the exercises was submaximal double-leg repetitive vertical jumps of 6–8 in., using minimal knee and hip action while emphasizing the calf action.   In the first week, each session included 60 foot-contacts, increasing to 140 foot-contacts per session by six weeks.   The outcome was a significant increases in running efficiency of 2-3% at paces in the range 5 – 6 min/Km.  A control group who continued with training as usual showed no increase in running efficiency.  Neither group exhibited increase in VO2max, or a significant increase in counter-move jump (CMJ) height.  The lack of significant increase in CMJ height was perhaps surprising, though in fact the group undergoing the plyometrics did exhibit a mean increase from 36 to 38 cm. This was not statistically significant, but the study probably lacked enough statistical power to detect the magnitude of change that might reasonably be expected.   Nonetheless, it was encouraging to see a small but significant and worthwhile improvement in running efficiency from a relatively modest plyometric program.

A more demanding program

Spurrs and colleagues employed a slightly more demanding 6 week plyometric program in more experienced athletes.  In the first three weeks, there were two plyometric session per week and then three sessions per week for the remaining three weeks.  The majority of the exercises were hops (single or double-leg), all performed at maximal effort.  Depth jumps were introduced in the fourth week.  The number of foot contacts was 60 per session in the first week and increased gradually up to 180 per session by the final week.  The gains were substantial.  Running efficiency increased by 6.5% at 5 min/Km and by 4% at 3.75 min/Km.  CMJ height increased significantly from 38cm to 43 cm and musculo-tendonous stiffness increased significantly by about 10% in each leg.  3Km time trial performance improved significantly by 2.7 % from 10:17 min to 10:10.  There were no changes in VO2max or lactate threshold.  A control group who continued with training as usual showed no significant changes in any measures.

My cautious program

Overall, the prospect for gain in efficiency and in race pace from a 6 week plyometric program looked promising.  However in light of my age and aching legs, it was clear that I should be cautious.  I decided that in contrast to the approach employed by Turner, who placed emphasis on the muscles acting around the ankle (especially gastrocnemius and soleus), I would  allow more flexion of hips and knees, since the large muscles (quads, hams and glutes) acting at these joints play a key role in running.  I therefore anticipated that I would need to employ somewhat greater jump heights.   A cautious introductory session with some hopping over 30cm high hurdles and drop jumps from 16 cm did not exacerbate the aches.  In fact, at that time, running was somewhat more painful than the plyometrics, so I decided that I would proceed with the plyometrics while cutting back the amount of running to around 10 Km per week.  I allowed three days recovery after each plyometric session, giving a total of three sessions every two weeks.  I interleaved a mildly demanding weight lifting session between plyometric sessions. To prevent complete loss of aerobic fitness, I replaced the some of the running with sessions on the elliptical cross trainer.

In the first plyometric session, after a gentle warm up that included body-weight squats, hip swings, calf-raises  and line-jumps  I did 5 sets of 2 double-leg  hops over 30cm hurdles and 5 sets of 5 drop jumps from 16 cm, rebounding to 16cm (a total of 35 foot contacts in the session).    This modest session left me with barely perceptible DOMS the next day.  In subsequent sessions I increased the numbers of hurdle hops; the depth of the drop jumps; and added single-leg hurdle hops.  By the end of the six weeks, each session included 5 sets of 7 double-leg hurdle hops (over 30cm hurdles); 5 sets of 5 single-leg hurdle hops on each leg (over 15 cm hurdles); and 5 sets of 5 drop jumps (from 30 cm rebounding to 30 cm  (total of 110 foot contacts in the session).   Although exact comparison with Turner’s program is not possible, I estimate that the early sessions in my program were less demanding than Turner’s,  but the later sessions were roughly equivalent.  However, whereas Turner’s athletes performed 18 sessions, I performed only 10 sessions over the six week period.    My CMJ height increased from 30 to 33 cm.   My other outcome measurement was horizontal distance covered in 5 consecutive double-leg hops.  This increased from 8.63 m to 9.08 m.

Unfortunately, there seemed little point in assessing the impact on my running performance.   Having done relatively little running in the 12 weeks since the half marathon, my aerobic fitness had deteriorated quite markedly, despite the elliptical sessions.   It was clear that my fitness at the end of September had been built on a very narrow base, and by mid-December, it had melted away.  However, one pleasing observation was that the persistent aches in my legs had almost entirely disappeared.


Overall, the six weeks of quite modest plyometrics  produced a definite increase in my jumping ability – comparable as far as can reasonably be estimated, with the  gains exhibited in the study by Turner, though somewhat less than achieved in the more demanding program employed by Spurrs.   Although I have no direct evidence of improved running efficiency or pace, the findings of both Turner and of Spurrs suggest that the improvement in jumping ability would probably have been enough to produce a worthwhile improvement in running efficiency, had I not lost aerobic fitness due to a drastic reduction in my volume of running.

At present I find myself in an ambiguous position.   I am somewhat dismayed by the severe and persistent aching in my legs that had developed in the summer during my preparation for the half marathon.   If I am to succeed in my plan to run a full marathon next year, I will have to build up the volume of running more gradually than had been feasible this year.  I will probably also include a higher proportion of elliptical cross-training.  However, it is pleasing to have demonstrated that I can achieve gains in jumping performance from a relatively modest program of plyometrics.  The gains appear comparable to those achieved by the young adults in the study by Turner, and perhaps even comparable to those achieved in the study by Spurrs, after allowing for the differences in volume and intensity of the plyometrics.  Furthermore, it will be interesting to see whether or not this moderate amount of plyometrics makes me more resistant to aching legs, in the long term.

Training in a fasted state

October 19, 2013

Nutrition for the runner is almost as important as training, but it is a topic that many athletes shy away from because it is bedevilled by crankiness.   In recent years, nutritional science has yielded a huge amount of potentially useful evidence about what nutrition is likely to work best in particular circumstances.  But the clamour of enthusiasts who seize upon a particular nutritional notion and assert that it is best for everyone makes it difficult to identify might be useful to a particular individual in particular circumstances.  Endurance athletes, sprinters and sumo wrestlers all practice the art of applying optimum muscular force at the right time, for the right duration, and in the right place.  There are similarities in the training that all must do, but also differences. Likewise, there are similarities in their nutritional requirements but also differences.   Just as with differences in training requirements, the differences in nutritional requirements depend not only on the type of sport but also on the individual’s genes, life history and the particular goal at the present time.  It is a complex topic.

In recent times there has been a great interest in the Paleo diet, a diet supposed to reflect the diet of our primitive ancestors. It is heavily biased towards the protein and fat available in meat, and biased away from carbohydrates, especially from cereals that have only been a staple since humans developed agriculture.   The Paleo diet has been given a little added spice by Tim Noakes’ endorsement of a similar diet, in a rather dramatic reversal of his prior recommendation of carbohydrates in ‘Lore of Running’, the book that has perhaps done more than any other to shape the opinions of runners since its first publication in 1991. It is of interest to note in his statement published in Runner’s World in 2012, Noakes was careful to state that on current evidence he only recommends the diet for individuals suffering what he described as carbohydrate resistance, a metabolic condition predisposing them to diabetes. Furthermore he emphasises that the proposed diet requires a long-term commitment for a life-time

In this post I will not focus on the issue of long term diet. That is an important topic for runners and much good data is now available, which I will return to in future posts.  Meanwhile I want to focus on the question of training in the fasted state, a question that both Robert Osfield and Eternal Fury have raised in their comments on my recent blog posted two weeks ago.   Both Robert and EF are advocates of training in the fasted state, and both are currently running very well.  Their accounts are of course only anecdotal evidence. Nonetheless, there is quite substantial body of relevant scientific research that is worth examining.

The question of training in a fasted state does overlap with the issue of long term diet and in particular, with the issue of the proportion of carbohydrates to fats.  It also raises the issue of differences between different types of carbohydrate: high glycaemic index (GI) carbohydrates which produce a rapid spike in blood glucose levels, and low GI carbohydrates which are absorbed more gradually; and also between different types of fats: especially the difference between omega-6 fatty acids which predominate in the typical Western diet, and omega-3 fatty acids, more abundant in both the putatively healthier Mediterranean and Japanese diets.     So the topic is already complex and the interpretation of the evidence must take account of this complexity

The metabolic requirements of endurance athletes

Our bodies store two main types of fuel: glycogen, which is stored in liver and muscle, and is the precursor of glucose; and fats which are stored in adipose tissue.  Glycogen stores are relatively limited and are typically exhausted by about 2 hours of running. Fat stores, even in the most slender of runners are virtually inexhaustible except in extreme starvation.   Muscle can utilise either fat or glucose when fuel is burned aerobically, but only glucose can be used to provide energy within consuming oxygen.  Hence muscles mainly utilise glucose at high intensities, when the demand for energy exceeds the available supply of oxygen.    For ultra marathon runners, running at aerobic intensities for many hours, fat is the preferable muscle fuel, not only because it is abundant but also because the brain requires glucose, making it crucial to conserve glycogen.   The mitochondrial enzymes that catalyse the combustion of fat are the same enzymes as catalyse the combustion of glucose.  It is therefore important to maximise the development of these enzymes for the effective use of either type of fuel.  However the special requirement for the ultra-marathoner is the ability to promote the mobilization of fats and the transport of fat into muscle cells, thereby promoting preferential utilization of fat.

For shorter endurance event (such as 5K or 10K) the efficient use of oxygen is paramount.  At the pace of these events, adrenalin levels promote mobilization of glucose from the glycogen stores, and glucose contributes a greater proportion to the fuel mix.   It is noteworthy that a little less oxygen is required to produce a given amount of energy from glucose than from fat, and hence the greater mobilization of glucose promotes more efficient utilization of oxygen.   Although the majority of the energy required at 5K or 10K pace is provided by aerobic metabolism, a small amount of anaerobic metabolism occurs, and the accumulation of the lactic acid produced by anaerobic metabolism is a limiting factor, so the 5K or 10 K runner also requires a well developed ability to metabolise lactate to minimise its accumulation.

In summary, both the ultra runner and the 5K/10K runner require well developed mitochondrial enzymes to enable muscle to burn either glucose or fat efficiently, ultra-marathoners also need to enhance the ability to mobilise fats and transport them into muscle cells, while 5K/10K runners requires well developed ability to metabolise lactate.    The marathon presents a unique combination of challenges. Typical race pace is not far below the level where anaerobic metabolism is appreciable, yet race duration is long enough to deplete glycogen supplies,  Therefore the marathoner requires well developed ability to mobilise and transport fats, highly developed mitochondria enzymes and also the capacity to metabolise lactate.

What role does the nature and timing of nutrition play in the development of these various metabolic capacities, and in particular, what role might training in a carbohydrate depleted state play?

The different goals of training and racing

It should be emphasized that optimum nutrition for training is likely to be different from that for racing.  There is no doubt that for endurance racing whatever the distance, it is crucial to ensure that glycogen stores do not become depleted, both to ensure adequate energy supply for the brain and to fuel increased muscle output required for hills or surges of increased pace.  Glycogen depletion is not likely to be a problem in short races, but beyond 30 Km, it becomes a major issue.  Many studies (reviewed by Burke) demonstrate that both adequate carbohydrate loading before the event and administration of carbohydrate during the event enhance performance, though these studies have not explicitly addressed the question of the timing and amount of carbohydrate that is optimal for an athlete who is well adapted to preferential use of fats.  It is probably best for the fat-adapted long distance runner to augment carbohydrates on race day sparingly to avoid undermining the advantage of preferential utilisation of fats.

Training in a glycogen-deleted state.

The potential benefits of training in a glycogen depleted state with the goal of enhancing fat mobilization, and also possibly enhancing mitochondrial enzymes that are involved in metabolism of either fat or glucose, have been debated for many years.  Various strategies for inducing carbohydrate depletion have been considered.  One strategy is to train twice a day without refuelling between sessions, thereby ensuring that glycogen stores are depleted at the start of the second session.  Perhaps the most impressive study using this strategy was performed by Hansen and colleagues from Copenhagen.  They trained the athletes’ knee extensors, applying different regimes for the two legs.  One leg was trained twice for one hour with a two hour rest between sessions, on alternate days, while the other leg was trained for one hour daily.  Thus both legs did the same total volume of training, but for one leg, half of the sessions were performed in a glycogen depleted state.   After 10 weeks of training, time until exhaustion when working at 90% of VO2 max exhibited a markedly greater increase in the leg that had trained in the glycogen depleted state compared with the other leg.  Mitochondrial enzymes also exhibited a greater increase in the leg trained during glycogen depletion.   Hansen concluded that training twice every second day might be superior to daily training.   Of course, the benefit of training twice on alternate days was not necessarily due to the glycogen depletion. It might have reflected other benefits of thorough recovery between sessions.

The findings from studies in which glycogen deletion is achieved by training after an overnight fast are less convincing.  On balance there is little consistent evidence for improved endurance performance.   There is however consistent evidence for the enhancement of enzymes involved in fat mobilization, and consistent evidence for a decrease in respiratory exchange ratio (relatively less carbon dioxide is produced compared with oxygen consumed) which is characteristic of fat metabolism (see the review by Burke).

The effects on mitochondrial enzymes are less consistent and might depend on the composition of the diet.  For example, Van Proeyen and colleagues from Leuven in Belgium demonstrated that in individuals consuming a carbohydrate rich diet, training in a fasting state improved both ability to utilise fats and also mitochondrial oxidative enzymes compared with training fuelled by carbohydrates before and during training.  However, in individuals consuming a high fat diet, the advantages of training in a fasted state on fat utilization were abolished.  Furthermore, fasted and non-fasted training produced similar improvements in time to exhaustion, while only non-fasted training produced a significant increase in VO2max.  Thus, for individuals on a high fat diet, the advantages of fasted training on ability to utilise fats and on aerobic development are lost; while non-fasted training actually produces a greater increase in VO2max.  It should be noted that the training intensity in the fasted and non-fasted groups was matched.  In light of the strong expectation that fasting would diminish the capacity for high intensity training, even greater gains in aerobic capacity might be expected from non-fasted training if exercise intensity was not controlled.

Potential disadvantages

At least in the absence of a fat rich diet, training in the fasted state does enhance both the development of fat utilization and the development of mitochondrial oxidative enzymes, but might it have disadvantages?   As already implied, it might impair the ability to perform well and thereby gain maximum benefit from a high intensity training session.  Perhaps even more important is the risk of excessive cortisol release.   Cortisol mobilizes helpful adaptations to stress, but excessive and prolonged cortisol release has adverse effects on many body tissues, and on the immune system.  Furthermore, as discussed in my post two weeks ago, there is evidence that endurance athletes tend to have sustained and potentially harmful increases in cortisol that are proportion to training volume. Hence, it is probably desirable to minimise elevation of cortisol during training.  Gleeson and colleagues demonstrated that exercising at 70% of maximal oxygen uptake for 60 minutes produced greater elevation of cortisol and potential disadvantageous changes in the immune system in individuals in whom glycogen had been depleted by three days of low carbohydrate intake.   Thus, the evidence is indirect, but suggests that training in a glycogen depleted state does create an increased risk of harmful elevation of cortisol.


Training in the fasted, glycogen depleted state is likely to enhance capacity to utilise fats, which is advantageous for an ultra-marathoner and perhaps also for marathoners.  Under some circumstances, it might also produce enhancement of aerobic enzymes.  However, a high fat diet abolishes these advantages of training in the fasted state.  Furthermore, training in a glycogen depleted state increases the risk of excessive elevation of cortisol during either intense or prolonged training sessions.  In addition, training in a glycogen depleted state would be expected to diminish performance in a high intensity training session and might thereby limit the benefits obtained from high intensity sessions.

Overall, I think that training in a fasted state has a very limited role to play, though might be advantageous for ultra-marathoners who wish to maximise capacity to utilise fats.  Although the alternative strategy of a high fat diet might nullify this advantage, it is necessary to evaluate the risks and benefits of a high fat diet.  I will address this issue in detail in a future post, but here, I will merely note that a substantial body of evidence does indicate that moderately high fat diets can be healthy, provided there is an approximately equal balance of omega-3 and omega-6 fatty acids, typical of the classic Mediterranean diet. In contrast, in most Western diets, there is an unhealthy preponderance of omega-6 fatty acids.  Furthermore, Venkatraman and colleagues have shown that increasing fats up to 40% of energy requirements, leads to increased endurance in healthy trained runners.

While there is strong evidence that avoiding glycogen depletion during races is crucial for peak performance, I am inclined to think that in many situations, the mild glycogen depletion achieved by avoiding carbohydrate consumption during training might be advantageous, because it is likely to enhance the capacity for fat utilization and might also promote mitochondrial enzyme development, especially in athletes who consume only moderate amounts of fat in their diet.   Therefore I do not consume carbohydrate during training (except to test strategies for refuelling during a race).  Furthermore, if training in a non-fasted state, it is worth considering what type of pre-training nutrition is optimal.  Sun and colleagues have demonstrated that a low glycaemic index (low GI) breakfast promotes utilization of fat rather than glucose during low and moderate intensity exercise.  A low GI meal minimises the spike in blood glucose but instead produces sustained release of glucose into the blood stream.  Therefore, I consider that a low GI breakfast is optimal for both training and also before a long race.

Too many long runs?

October 3, 2013

A few days reflection, a more detailed examination of my training logs, and an interesting discussion with Robert regarding nutrition in the comments on my recent post about the Robin Hood half marathon, have provided me with food for thought.  I think I have learned some useful lessons, but first of all, I should put that race into perspective.

Although I want to race well, and would like to once again run a creditable marathon, the underlying goal of my running is minimising the inexorable deterioration that accompanies aging.   Six years ago, I decided that I would train systematically for a half marathon.  I had been running regularly since the previous November, though averaging about only 8 Km (5 miles) per week.   At the beginning of March I started systematic training, initially building up volume on the elliptical cross trainer.  After 8 weeks my running pace at the second ventilatory threshold had increased from 6 min per Km to 5 min per Km.  I added increasing amounts of running and by mid-June, did a 5K time trial in 23:27.  I contemplated this ruefully in light of the times of my youth, but decided it was not too bad, and began to speculate whether a half marathon in 105 min might be possible.  I continued to do around 35 (equivalent) miles per week, including some elliptical sessions, and occasional longish runs of 15Km.  Then in August, the arthritis that had afflicted me in my 50’s made an unwelcome return.  At the time, we were on holiday in France, staying in a farm house and sleeping in the loft.  For a few days, I was forced to descend the steep steps from the loft each morning, shuffling on my bottom.   However, the storm abated as quickly as it had arrived, and about six weeks later, I ran the half marathon in 101:24.  That time remains my M60 PB.

This year, I have again trained been able to train regularly, disrupted only by an episode of arthritis early in the year. I have coped with a greater volume – about 46 (equivalent) miles per week over a period of 6 months.  However, by August, my pace at second ventilatory threshold was slower than 5 min/Km.  I did not attempt a 5Km time trial, but am certain that I would a have struggled to break 25 minutes.  A 105 min half marathon appeared to be an absurd goal.  However, based on previous experience I was hopeful that a few weeks of higher intensity, lower volume training would produce a major improvement.  On the day, this hope was partially justified by the fact that I was comfortably below the second ventilatory threshold while maintaining a pace 4:53 min/Km for the first two Km, on target for a time of 103 min.   But my legs were not coping well.   As described in my recent post, the pace ebbed away and I finished in 107:49, a little more than 6 minutes slower than my time six years ago.  Disappointing, but not really unexpected.  WAVA predicts a loss of a little over 1 minute per year for half marathon time at my age, so in fact I have deteriorated at almost the exact rate that WAVA predicts. Furthermore WAVA predictions are based on the performance of elderly runners who are not only naturally fast, but also are deteriorating less rapidly than average as they age. So the evidence indicates that I have at least slowed my rate of deterioration over 6 years to match that of the WAVA standard setters.  However, last years time of 101:50, which is my best WAVA graded performance of my 60′s suggests that I could do better.

This year’s campaign has several other bright spots.  I appeared to cope reasonable well with a volume of  46 miles per week for 6 months.  This bodes well for my plan to train for a marathon next year.  Secondly, I was pleased to find that I can still muster a competitive edge even when nearly exhausted.   With one Km to go, the sight of the swishing ponytail of a young lady who had passed me about 16 Km earlier provided the focus.  I covered the final Km in 4:56, a little faster than I had managed for any Km between 5 and 20 Km.  Having overtaken the young lady with the ponytail with 300m still to run, I subsequently overtook at least four other runners, all younger men, in a spirited run to the line.

105 metres to run and the young lady with the ponytail is now well behind (2nd right). I am in the blue vest and now closing on four young men.

150 metres to run and the young lady with the ponytail is now well behind (2nd right). I am in the blue vest and closing on four young men.

Less than 100 m to go and I am not the only one with an ‘awesome race face’.  The competitive juices are flowing.

Less than 100 m to go and I am not the only one with an ‘awesome race face’. The competitive juices are flowing.

20 m from the line.  The 4 young men are now behind, but I can’t quite catch another young lady, just out of camera view.

20 m from the line. The 4 young men are now behind, but I can’t quite catch another young lady, just out of camera view.

It appears that I am still able to muster the type 2B (fast-twitch) anaerobic fibres when the chips are down.  Unfortunately, type 2B’s can only function at maximum capacity for about 10 seconds.   Nonetheless, at least for a brief period, my type 2B’s were twitching fast enough.  The foot pod recorded a peak stride rate of 216 steps per minute.  But my peak step length was only 118 cm.   Thus, the final sprint confirms that the capacity of my leg muscles to generate a strong eccentric contraction is poor.   This is clearly one of the major limitations imposed by age.   I suspect it is because accumulated fibrous tissue obstructs dynamic stretching of the muscles.  During static stretching I can achieve almost as great a range of motion as I could achieve 55 years ago.    How can I recover my former dynamic range?  As outlined in my previous post, I think hill sprints are probably the best option.

Long runs

But my training log provides further food for thought.  My performance was substantailly worse this year than last year despite a 10% increase in training volume in the final six months.  It is necessary to look at the type of running, not only the volume.   The really striking difference was in the number of long runs.  This year I did 32 runs longer than 15 Km in those six months, many of them in the range 18-21 Km, whereas last year I did 16 runs longer than 15 Km in the corresponding period.  The increase in long runs was the outcome of a deliberate plan to develop better endurance this year.  In fact, I did improve my endurance substantially.  Early in April, one month into my half marathon campaign, I maintained a pace of 6:15 /Km and a heart rate of 740 beats/Km during a typical 16 Km run.  Five months later, I did a 19 Km run at similar effort level and at a pace of 5:43 /Km, with a heart rate of 697 beats/Km.

But is it possible to do too many long runs, even at an easy pace?  Dudley’s well known study of rats training on a wheel for various durations and intensities, demonstrated that aerobic capacity increases with increasing duration of running, but only up to a certain limit, that depends on intensity.  The duration for optimal gain was greatest at low intensities, at paces where most of the work is done by slow twitch fibres.  But even at low intensity, there was no additional gain in aerobic capacity beyond about 90 minutes of training.    The physiology of muscle fibres in humans is quite similar to rats, though proportions of fibre types differ both within and between species.  Nonetheless, despite probable small differences, it is unlikely in either rats or man, that training beyond around 90 minutes will produce further improvement in aerobic capacity.  There might of course be other benefits, including conditioning of connective tissues and improving the balance between consumption of fat and glucose.  But could there be penalties?


For several years the debate between cross-fit enthusiasts and endurance runners has focussed on the potentially harmful effects of cortisol. In the short term, increase in cortisol mobilizes the body’s resources to deal with stress. In particular, it mobilizes glucose to fuel brain and muscle; and limits inflammation.  It should be noted that the brain is the higher priority; although blood glucose levels are increased, cortisol inhibits access to the glut4 transporter molecules in muscle cell membranes that transport glucose into the muscle, thereby ensuring preferential supply to the brain.   But perhaps more importantly for the rpesent discussion, sustained increase in cortisol has a range of harmful effects, including destruction of muscle and weakening of immune defences.  Cortisol rises steadily during long duration exercise.  Typically the level increases to around 220% of normal levels during a marathon.  The crucial issue is: how long is this increase sustained?  In a fit person, the level returns near to baseline within a few hours.  However, in the presence of other stresses, it can remain appreciably elevated for several days.  Until recently, the debate between cross-fitters and endurance runners has remained stalemated over the issue of whether or not typical endurance training programs produce a significant sustained increase in cortisol.

However in 2012, Skoluda and colleagues published the results of a thought-provoking study.  They measured cortisol levels in hair samples in athletes.  Levels of cortisol in hair, unlike levels in blood or saliva, provide a good index of sustained levels.  They found that in a sample of 304 endurance athletes, fairly representative of committed recreational runners, levels of cortisol, in hair were almost 50 % greater than in a reasonably well matched control group.   Furthermore the magnitude of the increase was greater in those with greater weekly training volume.  The increase was greater in marathon runners than in half marathoners, though both groups had values that were significantly increased compared with controls.  Typically a training volume of 70 Km/week (a little lower than my average of 74 Km/week) was associated with a 1.8 fold increase in sustained level of cortisol.  The health consequences of an increase of this magnitude are unclear though such an increase might plausibly result in greater risk of upper respiratory tract infections and even perhaps add to the risk of atherosclerosis and myocardial infarction.   There is evidence for increase in atherosclerosis among male multi-marathoners, as I have discussed previously.  Furthermore, the elevated cortisol levels might inhibit protein synthesis in muscles and limit any gain in strength.

It should be noted that increases in cortisol during exercise are usually less in well trained athletes, suggesting that problems due to cortisol might by ameliorated by a gradual increase in training volume. On the other hand, running in a glycogen depleted state would be expected to increase cortisol levels.  Therefore, I remain sceptical of the wisdom of training in a carbohydrate-depleted state.  In the discussion following my most recent post, Robert has raised some interesting points related to his positive experiences following changes in both the type and timing of his nutrition, including doing long runs without breakfast.  He is running very well at present, though it is perhaps noteworthy that his total training volume has been relatively low this year compared with previous years, and hence, sustained cortisol levels would not be expected.

Total volume or length of long runs?

Although Skoluda did not attempt to disentangle the effects of total weekly training volume from length or frequency of long runs, the evidence that cortisol rises steadily during a long run raises the possibility that it is the length and frequency of long runs that is the main contributor to sustained elevation of cortisol.  When taken together with the evidence that gains in aerobic capacity are likely to be small after 90 minutes of training, I think it is quite plausible that the large number of long runs in my program this year not only contributed to a relatively slow gain in aerobic fitness, but might also have produced a sustained increase in cortisol that impeded the development of strength.   Although I intend to prepare for a marathon next year, I will be more judicious in planning the frequency of long runs.

Robin Hood Half Marathon and plans for the future

September 30, 2013

I lined up for the Robin Hood half marathon yesterday hopeful, but uncertain.  I had a successful six months of training behind me.  By using of the sub-maximal tests described in my posts in June and July to monitor for signs of over-training, I had managed to achieve a 10 % greater training volume than I achieved in the corresponding six months last year.  My aging legs had coped well.  My aerobic capacity had improved slowly but steadily throughout the six months, and furthermore I had managed to do a large number of training runs longer than 15Km, many of them in the range 18-21Km, so it was reasonable to expect that my endurance would be adequate for a half marathon.

In several of these long runs I had increased pace progressively, aiming to reach something near race pace in the final few Km.    However, the disappointing observation was that I had struggled to achieve a pace any faster than 5 min/Km in these runs.  On the one occasion when I achieved even this modest pace, my breathing and heart rate indicated I was already beyond the anaerobic threshold.  Simple physiology indicated that a 100 minute target for the half marathon (4:44 /Km) was unreasonable, but I pinned some hopes on the fact that in last year’s Robin Hood half marathon, I had run far better in the race than prior training suggested was possible.  While my aerobic capacity wasn’t quite as good this year, I was confident that my endurance was better.  So I planned to start at around 4:50 min/Km and adjust pace according to how well I was coping.

The weather was ideal for distance running: broken light cloud with bursts of sunshine and a cooling breeze.  Within the first few hundred metres I was a little surprised to see my heart rate shoot up to an alarming level and wondered whether there might be an impending cardiac problem.  However it soon settled to a reasonable level.   Perhaps I was a little more nervous about this race than usual.   I covered the first two Km at 4:53 min /Km (103 min HM pace).   I felt much more comfortable than I had felt at a similar  pace in training, but it was clear by 3 Km that I would not be able to maintain that pace for much longer.  My breathing was still quite comfortable but my legs were not coping.  In an attempt to reduce the impact forces on my legs, I increased cadence to over 200 steps per min, but my stride gradually shortened further and pace gradually ebbed away.

Although it was clear in the later stages that I would be far short of my target, and indeed had no chance of even achieving 105 minutes, I pushed on as fast as my failing legs would carry me in the final few Km.  However the increased effort was to little avail. As each runner went by I tried to lift my pace, but despite my attempts, each one forged inexorably ahead. Then with a little over 1 Km to go I spotted a young lady with a pink top and swishing pony tail who had passed me about 16Km earlier. The gap was slowly closing, so I had a target for the final Km. I caught her as we climbed up to the flood defence embankment with a few hundred metres to run. She defended strongly for a few metres but I was able to find a little extra drive. So despite being passed by many in the final stages, I claimed one scalp at the end.   My finishing time was 107:49

Afterwards I felt pretty wobbly and a couple of first aiders were quite solicitous for my welfare.  I managed to stay upright though I did need to steady myself against a tent pole.  I wasn’t in danger of fainting; I was simply exhausted.   So what does the future hold? I trained about as well as I could have for this event, but I am not yet ready to abandon hope of pushing back the tide of advancing years.  Perhaps on another day I might have achieved a time better by a few minutes, but if I want to run substantially faster in future, I need to carefully evaluate my strategy.

Aerobic capacity

It is important to note that my aerobic fitness did improve steadily during the six month of training.  In the final sub-maximal test, done during the taper, I achieved 650 heart beats/Km, whereas 6 month previously, shortly after resuming training after a bout of arthritis, the rate was nearer 750 beats/Km.    But the improvement throughout the six months had been painfully slow.  In 2010, when the year had started with a bout of arthritis similar to this year, I had made greater improvement in aerobic capacity in less than 3 months, with a much lower volume of training at a higher intensity.  However that year, my half marathon campaign was stymied by a several illnesses in the summer.    Nonetheless the progress in spring of that year indicates that higher intensity training would be likely to produce a more rapid gain in aerobic capacity.

The phenomenal marathon performances of Ed Whitlock, who does a very large volume of low intensity training, spiced up with fairly regular races, demonstrates that a program based largely on low intensity training can work well.  However, despite the relatively satisfying demonstration that I could cope with a moderate volume of training this year, it appears that I am unable to cope with anything like the volume of training that Ed Whitlock does.  He doesn’t record distances, but runs for several hours each day at an easy pace.  If I increase my training volume to 50 miles in a week, even at an easy pace, I experience rapidly accumulating exhaustion.  So, if I am to produce substantial further improvement in aerobic capacity, greater intensity offers the best prospect.

As I have described on several occasions previously, there is good evidence that high intensity interval training can produce increases in aerobic capacity, including increases in aerobic enzymes and muscle capillary density.  At this stage, I am very tempted to try HIIT for at least a few weeks, as soon as I have recovered from yesterday’s race, to see how well I cope with it.

Muscle power

But there is little doubt that yesterday the principle limitation was my lack of leg muscle power.    I had reached a similar conclusion last year.   Loss of muscular strength is one of the most overt problems of the elderly, and therefore at that stage, the logical step was a program of weight training to increase strength.  Since squats provide a very good ‘whole body’ workout, with particular benefits for legs and trunk, I embarked on a program of squats augmented by dead lifts.  In the final months of the year, I made major gains in strength, increasing my 5 repetition maximum (5RM) for squats from a little over half my body weight to more than 160% of body weight in a period of three months.

I had intended to follow that lifting with a program of plyometrics to increase my capacity to handle the eccentric loads that the leg muscles bear at footfall when running.  Unfortunately, the episode of arthritis confounded that plan.  Since recovering from arthritis, I have continued a maintenance program of squats, and my 5RM has only deteriorated only a little.  However, apart from a small amount of trampolining, I have not dared to introduce plyometrics for fear of stressing my fragile joints.

Eccentric strength

The crucial test of eccentric strength is hopping.  Unfortunately, the distance I can cover in five hops has deteriorated by about 20 percent compared with three years ago.  It is interesting to note that subsequent to the program of weight lifting, my performances on the elliptical cross trainer have been better than at any time in the past three years.  Since the elliptical requires a leg action similar to running, apart from a minimal requirement for eccentric contraction, it is almost certain that the increased strength has helped me perform better on the elliptical, but has had little impact on my running because there has been little improvement in eccentric muscle strength.

So the major challenge is to find a way to increase eccentric muscle strength without placing too much stress on my knees.  I will continue with squats and dead lifts, and probably also add hang cleans as these are good for developing power in the upper leg muscles, but  this program is unlikely to provide the eccentric strength required for powerful running.  At this stage, hill sprints appear to offer the best option.

Next steps

I have not yet formulated a detailed plan for the winter, but it will include a trial of HIIT and also lots of hill sprinting.   Next year I want to focus on preparing for a marathon in the autumn, so I will begin working on endurance in the spring.   Although the half marathon will not be a key target, I will probably attempt a half marathon sometime in the spring.  I will not set a specific goal at this stage, but think it is reasonable to hope that a time somewhat better than yesterday’s performance will be possible.

Responses to training and to over-training

September 25, 2013

I am now tapering for the Robin Hood half marathon, five days away.  After a frustrating start to the year, in which a recurrence of arthritis limited my training for a few months, I have been able to train consistently for six months.    I have achieved a greater training volume in those six months than I managed in the equivalent period last year, but frustratingly, my pace during tempo runs and progressive runs is slower this year than last year.    In the event, last year I performed better than appeared possible in the light of my prior training paces, though at the cost of a  somewhat painful final few kilometres.  Again this year I will be hoping that I can lift myself to a higher level on race day.  Despite the lower level of aerobic fitness this year, I am hoping that the greater training volume will have produced greater endurance.   So I will be approaching the race with modest optimism that I can achieve a time near to last year’s time.

However, Sunday’s race is merely a stage in my campaign to run a respectable marathon at age 70.  At this stage it would be premature to estimate a target time for a marathon in three years time.  This year’s Half Marathon will provide something of a guide, though in fact my most important goal this year has been to establish that I can maintain an adequate training volume over a period of 6 months.  Because my aging legs cannot cope with too much stress, I do about 20% of my training on the elliptical cross trainer.   In the past 6 months, I have averaged 36 miles of running per week, together with an additional 1000 Kcal/week on the elliptical (equivalent to approximately 10 miles/week), giving an average weekly training volume equivalent to 46 miles per week.   Although modest in comparison with a volume exceeding 100 mpw achieved by many younger marathoners, the key question is how to determine  the optimum amount for me.    The short answer is the that optimum amount is the amount that maximizes my response to training in the short term while building a base for future years.

What determines the response to training?

Four things determine the benefit you get from training.

  1. Genes
  2. Life-time training experience
  3. The type, intensity and volume of the training
  4. Current level of stress.


There is little that we can do about our genes, but it is nonetheless, worthwhile reviewing the issue of genes briefly.  The marathon performances of my younger days suggest that I was blessed with genes providing at least a moderate natural facility for distance running and also with the capacity to profit from training.

However in my present situation there is a third aspect of genetic endowment that matters: my ability to withstand the ravages of age.  My parents both enjoyed moderately good health into their 80’s, so I have probably at least an averagely good selection of genes for longevity.  The evidence from my own health so far is equivocal.  Throughout my sixties I have suffered several health problems that have confounded any attempt to answer the question of how the tissues of my body are aging.  These minor illnesses in themselves might be an indicator of increasing vulnerability to deterioration, but give little indication of widespread deterioration.  In light of the fact that I have been able to train consistently for six months, my performance next Sunday will be potentially a good measure of the underlying rate of deterioration, uncontaminated by illness.    To match the rate of deterioration predicted by WAVA, I can afford to drop 1 minute compared to last year’s HM time of 101:50. On present form, even 102:50 will be a challenge.  However, if possible I would really like to set the clock back at least a little.   My gold standard target is 100 minutes and silver standard is last year’s time: 101:50, though realistically I should be very pleased even to achieve 102:50.

Life-time training experience

In the short term, there is little I can do to alter life-time training experience, but in regard to the medium term future, there are important issues to consider.  I suspect that running to and from school over 60 years ago, got me off to a good start.   However the more pressing issue at my current age is the question of whether a large annual training volume at this stage will actually hasten deterioration.  Excessive training can lead to chronic inflammation that is likely to damage tissues, possibly irreversibly.   It is likely that a range of factors, including not only genes and past experience but also current lifestyle factors, especially diet, influence this.  Thus, the question of how much training an individual can tolerate is likely to differ between individuals but is not necessarily immutable.   But whatever my current ability to tolerate training might be, monitoring response to training to detect signs of over-training is likely to be crucial.  I will return to this when addressing the effect stress in greater detail.

The type, intensity and volume of the training

Not only volume of training, but also type and intensity play a key role in shaping both the  immediate response and also the long term effects of training.  The pros and cons of different training regimes is too large a topic to deal with here, but it is perhaps pertinent to note that many athletes who have enjoyed years of high-level performance adopted a periodised program along the lines advocated by Arthur Lydiard, with a limited period of high intensity training and competition following a period of base-building in which the emphasis is on large volume of training at modest or low intensity.   I started my current HM campaign with a period of Lydiard-style base-building, and am confident that this was beneficial

Current level of stress

Again we are brought back to the key issue of stress.  As already discussed, avoiding cumulative tissue damage due to chronic inflammation is likely to be a key to the longevity of an individual’s running career.  It is also a key determinant of the short term response to training.

It is widely recognised that the benefits of training arise from a training stress followed by an adaptive response during the recovery period.  So stress is an essential element of training.  The stress includes microscopic local trauma to body tissues including muscle fibres and other connective tissues, and also increases in stress hormones that exert a widespread influence throughout the body.

Microscopic damage to muscle fibres activates satellite cells, which are a type of stem cell that when activated combine with muscle fibres to extend and strengthen them.   Thus in the short term heavy exercise results in loss of strength, but provided recovery between sessions is adequate, there is an overall upward progression.   On the other hand, if recovery is not adequate, there is a risk of a downward spiral.

In the case  of the hormonal responses, the increase in the stress hormone cortisol  promotes a physiological state that mobilises body resources in a way that is helpful in the short term, but potentially damaging in the long term.  The benefical short term effects include mobilisation of glucose and fats to fuel activity, but in the longer term, the result is muscle breakdown and deposition of fat.  Cortisol has anti-inflammatory effects which in moderation tend to be helpful, but if excessive or prolonged, weaken the immune system.  The mechanisms that determine the balance between the beneficial and harmful effects of inflammation are complex and remain something of a mystery.  But, at least one thing is clear: sustained stress leads to damage to many tissues of the body.  Fat is deposited around the viscera; chronic inflammation damages heart and skeletal muscle.  Adequate recovery is essential, both for the sake of a constructive medium term training benefit, and also for long term health and fitness.

Monitoring stress

Therefore, during the past six months, as I have attempted to establish the limit of training volume and intensity that my body can cope with, I have performed the sub-maximal tests described in my posts on 25th June  and 17th July 2013, on a weekly basis.  Apart from one episode early in the year, when I had increased the training load too rapidly, I have avoided the suppression of heart rate at sub-maximal effort which is a warning of impending over-training.  However on numerous occasions I have observed a moderate increase in heart rate at sub-maximal work rates, which I interpret as a sign of accumulating stress.  In response to this sign of accumulating stress I have avoided demanding training session for a few days, and the signs of stress have resolved.

The apparently clear-cut benefit of this strategy for regulating training stress is that this year, I have managed to cope with a training volume over the 6 months from April to September that is about 17% higher than in the equivalent period last year.   I am optimistic that this will stand me in good stead next year when I intend to train for a marathon.  However, as outlined in the introduction, the somewhat disappointing outcome is that I appear to have a lower level of aerobic fitness (indicated by heart beats/km at a given pace in the aerobic zone) than at this time last year.   Possibly this is due to a lower initial level of fitness arising from the disruption of training in the early months of this year.  Alternatively, perhaps in my determination to make up for lost time, I might have pushed myself too close to my limit and therefore gained less benefit from the training.  However, provided I have not seriously exceeded the limit, it is not unreasonable to hope that I might experience a similar improvement in performance during the taper this year as last year, and in addition will be able to draw upon enhanced endurance based on the greater training volume.   I will start the half marathon on Sunday with the goal of testing this optimistic speculation.

Ewen, I will do my best to earn that mansion in Forrest for you, but I fear that your garden shed might be at risk.

Does anaerobic training damage aerobic fitness?

August 5, 2013

I am now well into the final phase of race-specific preparation for the Robin Hood half marathon in September.  I have added two sessions per week of moderately high intensity training, such as intervals or a tempo run, while making a slight reduction in over-all training volume relative to the base-building phase that was dominated by low intensity running.   My most recent sub-maximal tests show no improvement in beats/Km over the past month.  Perhaps this is a realistic indication that my fitness has peaked – though well below my target level.  However there is an alternative explanation.  This brings us back to a long-standing debate: does anaerobic training damage aerobic fitness?

There is at least one circumstance in which this is unequivocally true – the state of over-training which I will address in my next post, but at present, testing provides no evidence that I am over-trained.  I hope that the current apparent stasis in development of aerobic fitness is actually a sign of continuing improvement  in race fitness.  The explanation demands laying bare some of the misconceptions that surround the concept of anaerobic fitness.  But first it is necessary to review the much better understood concept of aerobic fitness

Aerobic fitness

Aerobic fitness is the capacity to fuel muscle contraction by means of the combustion of fuel – either glucose or fat – in the presence of oxygen, to produce carbon dioxide while transferring chemical energy  to create  high energy phosphate bonds in molecules of adenosine triphosphate (ATP), which in turn fuels muscle contraction.   The key steps of this process of oxidative metabolism occur in mitochondria within muscle cells, especially in slow twitch muscle fibres which are capable of generating a modest power output by repeated contraction over a period of hours, before they become fatigued.  The three major physiological adaptations that are required to establish aerobic fitness are increase in mitochondrial oxidative enzymes, increase in the density of capillaries delivering oxygenated blood to the muscle cells, and increased pumping capacity of the heart.  As was first clearly demonstrated by Arthur Lydiard , often described as the ‘father of jogging’ but also coach of Olympic champions including Peter Snell, gold medallist at 800m in Rome and at 800m and 1500m in Tokyo,  aerobic fitness can be established by a large volume of low intensity running.   However it should also be noted that at least some aspects of aerobic fitness, especially the development of mitochondrial oxidative enzymes, can also be enhanced by high intensity interval training, as clearly demonstrated by Martin Gibala and colleagues, at McMaster University in Ontario.

Anaerobic fitness

Anaerobc fitness is the capacity to fuel muscle contraction by metabolic processes that do not require oxygen.  There are two major anaerobic processes: glycolysis, which generates ATP from glucose in a manner that extracts only a small fraction of the energy available in glucose, by converting it to lactic acid; and the phosphocreatine system  which employs  the chemical energy contained in high energy phosphate bonds of phosphocreatine to generate ATP.   The phosphocreatine system can release energy very rapidly but the total capacity of the system is small, typically fuelling intense muscle contraction for a period of less than 10 seconds. Therefore this energy source is mainly of relevance to sprinting, and plays an almost negligible part in distance running.  However, the production of lactate from glucose via glycolysis plays a crucial, but ill-understood role, in distance running.

Anaerobic capacity

The term anaerobic capacity is used by different people in different ways.  Simon Green from University of Western Sydney wrote an interesting article discussing the various ways the term has been used, and the confusion that has arisen from this.  In a paper written in collaboration with his former mentor, Professor Brian Dawson from University of Western Australia, Green  offered the following definition: Anaerobic capacity is defined as the maximal amount of adenosine triphosphate resynthesized via anaerobic metabolism (by the whole organism) during a specific mode of short-duration maximal exercise.

I think that is a helpful definition though in my view it undervalues the important role of anaerobic metabolism in setting the limits on performance during events ranging from 800m to marathon.   At least for the distance runner, the capacity to sustain a minor contribution from anaerobic metabolism over a time scale of order of an hour or two, is important.  While the aerobic capacity produced by a large volume of low intensity running might be enough to transform a typical couch potato unable to run continuously for 5K into a 3 hour marathoner, I think it is likely that the ability to squeeze extra power from anaerobic metabolism makes a significant contribution to the difference between a 2:10 marathoner and a 2:05 marathoner, and indeed  allows recreational  athletes to perform at their best possible level across any distance from 800m to marathon.

How is anaerobic capacity developed by training?  First we must consider the mechanisms by which anaerobic capacity might be increased:

One major mechanism is via hypertrophy of type 2 (fast twitch fibres) which are specialised for anaerobic metabolism  But other processes are important.  These include the ability to remove lactic acid, since the factor that limits anaerobic energy production is the accumulation of acidity.  (Lactic acid is a combination of lactate ions and hydrogen ions.  The hydrogen ions make it an acid.)  When acid levels in muscle become too high, muscle contraction ceases.    Removal of lactic acid is achieved by the Cori cycle, which regenerates glucose from lactate in the liver.   Furthermore, muscle, heart and even brain, can metabolise lactate directly to produce energy via conversion back to pyruvate which is an intermediate molecule on the pathway to the oxidative metabolism of glucose.   In the presence of oxygen, pyruvate undergoes oxidative metabolism in mitochondria generating ATP and fuelling intracelluar processes including muscle contraction.

A third mechanism by which anaerobic metabolism can be enhanced is by increasing the ability to tolerate acidosis.  This mechanism might operate via either an increased capacity of muscle to buffer acidity or an increase in tolerance of acidity mediated by the brain. Maybe this latter mechanism could simply be regarded as an increase in mental  toughness produced by anaerobic training, though I believe that the mechanism by which the brain regulates tolerance should not be dismissed merely as mental toughness. I believe that the regulation of tolerance plays a cardinal role in the over-training syndrome. But that is an issue I will defer to my next post.

In general, any form of exercise that involves rapid consumption of a large amount of energy will enhance anaerobic capacity.  For example explosive activities such as sprinting will promote the development of type 2 fibres.    In addition, activities that entail sustained exposure to moderate levels of lactate, such as intervals with short recovery or tempo running, would be expected to increase the body’s capacity to utilise and thereby dissipate the accumulated lactate.

Anaerobic metabolism during distance running

Because anaerobic metabolism provides a rapidly accessible but transient supply of energy, whereas aerobic metabolism provides a slow but sustainable supply, the proportion of total energy provided by anaerobic metabolism decreases with duration of activity.  For intense activity lasting about 90 seconds, the amount of energy provided by anaerobic metabolism is approximately equal to that provided by aerobic metabolism, but for longer events, aerobic metabolism is the dominant source.   However, for races over distances from 5km to marathon the pace is not far from lactate threshold – the level where lactate begins to accumulate remorselessly if exercise is sustained.  A 5K race is run a little above lactate threshold because modest accumulation of lactate can be tolerated for 15-20 minutes. In contrast, a marathon is run a little below lactate threshold, but nonetheless in a zone where lactate level is appreciably above resting level, though relatively stable because the rate of dissipation matches the rate of production.    Thus even in the marathon, a small portion of power is derived from anaerobic metabolism but perhaps even more importantly, the limit on marathon pace is determined by the ability to dissipate acidity.  Enhancement of this ability is crucial for maximal marathon performance.

What is the effect on anaerobic training on fitness for distance racing?

The black line in figure 1 is a schematic represention of the way in which lactate level might increases as pace increases, at the beginning of a training block.   As pace increases beyond a vaguely defined threshold known as the aerobic threshold, lactate level rises slightly, typically exceeding 2 mMol, but then remains nearly constant as pace increases up to the point where lactate begins to rise sharply – the lactate threshold.   Between the aerobic threshold and lactate threshold, a modest amount of anaerobic metabolism generates lactic acid but the level remains failry stable because the body is able to dissipate the lactic acid as fast as it is produced.  A crucial feature relevant to anaerobic metabolism during distance running is the fact that there is no sharply defined anaerobic threshold.  Anaerobic metabolism contributes a small but steadily increasing amount to total energy production as pace increases across the entire range.  As the runner approaches the lactate threshold, the upward trend of lactate level increases.  When the rate of production overwhelms the ability to dissipate the lactic acid, the concentration of lactate exhbits a marked upswing.

The green line represents the increase in lactate after a block of low intensity, high volume training (i.e. typcial aerobic training).  Mitochondrial enzymes and the density of capillaries around slow twitch fibres have increased, favouring aerobic metabolism. The decreased proportion of energy derived from anaerobic metabolism leads to a slower rise in lactate, so the lactate threshold occurs at a higher pace.  It would be expected that marathon performance would be improved because the runner could maintain a faster pace without remorseless accumulation of acidity.  Furthermore, since running at low intensity favours the metabolism of fat relative to glucose, this training would be expected to increase capacity to metabolise fat and hence, during the marathon, glucose would be conserved.  However, it should be noted that an athlete who has already enaged in extensive base-building prior to the beginning of the training block, there will be little scope for futher aerobic development and the rightward shift of the curve is likley to be curtailed.

Figure 1: Schematic illustration of changes of the curve representing increase in lactate level from the baseline at the beginning of training block (black-line) produced by three types of training. The horizontal dashed line represent the lactate level tolerable for the duration of a marathon. Vertical lines represent marathon pace after various types of training  Green: low intensity high volume training shifts the curve rightwards, increasing marathon pace. However if there is near full aerobic aerobic development at baseline, the increase will be trivial. Red: sprints with full recovery produce hypertrophy of type 2 fibres, shifting the curve to the left thereby decreasing marathon pace though middle distance performance might be increased. Blue: intervals and tempo sessions lead to hypertrophy of type 2 fibres, increasing lactate at mid-aerobic paces, and also increase aerobic capacity, producing modest increase in marathon pace.

Figure 1: Schematic illustration of changes of the curve representing increase in lactate level with pace, from the baseline curve at the beginning of training block (black-line) produced by three types of training. The horizontal dashed line represents the lactate level tolerable for the duration of a marathon. Vertical lines represent marathon pace after various types of training
Green: low intensity high volume training shifts the curve rightwards, increasing marathon pace. However if there is near full aerobic development at baseline, the increase will be trivial.
Red: sprints with full recovery produce hypertrophy of type 2 fibres, shifting the curve to the left thereby decreasing marathon pace though middle distance performance might be increased.
Blue: intervals and tempo sessions lead to hypertrophy of type 2 fibres, increasing lactate at mid-aerobic paces, and also increase aerobic capacity, producing modest increase in marathon pace.

The red line represents the changes in lactate after a block of training consisting mainly of short, explosive bursts of activity separated by full recovery – typical of sprint training. From the point of view of energy production and utilization, the most important change will be hypertrophy of type 2b (anaerobic fast twitch) fibres. As these fibres have very limited capacity for aerobic metabolism, anaerobic metabolism will have increased relative to aerobic metabolism and the lactate threshold will be reached at a slower pace.  On the other hand, it is probable that the peak attainable level of lactate will have increased.   Because at least moderate elevation of lactate can be tolerated for periods of up to 15 minutes or so, it is quite likely that performance over middle distance events will have been enhanced by this block of training, but marathon performance is likely to have deteriorated. In this sense it might be claimed that the training block has impaired aerobic performance, though there had not necessarily been any intrinsic damage of the aerobic capacity itself.  Provided any conversion of slow twitch fibres to fast twitch fibres is negligible, the ability of muscle to metabolise fuel aerobically has not suffered sustained damage. In summary the athlete is likely to have enhanced fitness for middle distance events but impaired marathon performance.

What happens if the training block was focussed on tempo training or interval training during which effort epochs are separated by short recovery periods.  The likely effect is depicted by the blue line.   Some development of fast twitch fibres will occur.  These will be mainly aerobic fast twitch fibres (type 2a) which are capable of aerobic metabolism but derive a smaller proportion of energy form aerobic metabolism than slow twitch fibres.  Hence, production of lactate will be higher in the zone between aerobic threshold and the lactate threshold, than at the start of the block (black line.)  However, due to the sustained levels of lactate throughout the tempo sessions and interval sessions, capacity to handle lactate will be enhanced.   So the sharp upward turn of lactate level will be deferred to a faster pace.  The athlete is likely to be fitter for both middle distance and long distance racing, even up to marathon distance, than at the beginning of the training block.  However, he/she is unlikely to be as fit for a marathon as a runner who engaged in effective low intensity, high volume training, represented by the green line.

Does this mean that a marathon runner would be best advised to devote their training time to running at low intensity for as high a volume as time permits?   For a novice runner, preparing for their first marathon, I think that is the correct conclusion, though it should be noted that even high volume low intensity training can lead to over-training, as I will discuss in my next post, so there are limits on the optimum  volume.    However, for an experienced runner with a history of several years of regular training, the situation is different.  At the beginning of the pre-marathon training block, an experienced runner is likely to already have well developed capillary density around the slow twitch muscle fibres and mitochondrial oxidative enzymes.  Thus, the scope for the type of change depicted by the rightward shift from the black line to the green line in figure 1 is curtailed, and it is likely that a training strategy that includes a substantial amount of interval and/or tempo training is preferable, leading to an increase in type 2 fibres and also a small rightward shift of the lactate curve, thereby maximising race pace.

How does this analysis match the recommendations of expert coaches?

Let us consider in turn the training strategies recommeded by six different coaching schools, ordered according to proportion of high intensity training.


Phil Maffetone recommends that the majority of training s done at easy paces where ‘easy’ is defined as slower than the pace required to produce the heart rate which he calls the Maximum Aerobic Function (MAF) heart rate.  MAF heart rate is defined as (180 – age) modified by some quasi-arbitrary adjustments allowing for experience and age.   At least for the novice non-elderly runner, the  MAF heart rate is likely to be comfortably below lactate threshold.  The analysis depicted in figure 1 suggests that Maffetone training is ideal for the novice.  For a more experienced athlete, the MAF heart rate is increased by 5 beats, and for an experienced elderly athlete, it is in fact increased by total of 15 beats per minute.   If I were to ignore a subtraction on account of my recent bout of arthritis, my MAF heart rate would be in a zone where I would expect to be generating appreciable lactic acid, so even training at the MAF heart rate is likley to produce some anaerobic development.


The late John ‘Hadd’ Walsh recommended a high volume of low intensity running at or below 75% of maximum heart rate, where lactate accumulation is slight, and in addition, one or two sub-lactate threshold runs of approximately an hour duration each week, during base-building.  The pace of the sub-lactate threshold runs is the maximum pace at which a steady heart rate can be maintained for an hour.  Such sessions would be expected  to produce substantial enhancement of capacity to handle lactate, and hence, increase anaerobic capacity.  Furthermore Hadd recommended a period of race specific training after base-building in which moderately intense session were introduced.  Thus Hadd training is likely to be suitable for a moderately  experienced athlete.  Nonetheless, I consider that an experienced athlete is unlikely to achieve their absolutely peak performance unless the base-building is followed by race-specific  training that is sufficiently intense to develop type 2a fibres.


Arthur Lydiard’s  base-building program was similar to that recommended  Hadd, and indeed probably provided  the foundation on which Hadd subsequently constructed his base-building program.   Lydiard  recommended a large volume of low intensity training, but prescribed sessions at one of three different effort levels.  A ‘quarter effort’ is a session that could easily be repeated again immediately.  A half-effort session could be repeated the next day while a three-quarter effort sessions requires at least a full day of recovery.    It is not certain how Lydiard’s three quarter effort session compares with Hadd’s sub-lactate threshold session, but from the available descriptions of the Waitakere hill run that Lydiard’s athletes performed on Sunday morning, I suspect that for  Lydiard’s elite athletes the three quarter effort session was more demanding than Hadd’s sub-lactate threshold session.  Lydiard’s stable of Olympic medal winners, over distances from 800m to marathon, demonstrates that his program was capable of producing world-beating performances, at least in the middle years of the last century.

Pfitzinger & Douglas

Pfitzinger and Douglas offer a range of marathon training plans, differing in weekly mileage but based on similar underlying physiological principles.  Their 18 week 50-70 mpw plan assumes that the athlete has already done a substantial amount of base-building. The plan itself is divided into four mesocycles.  The first mesocycle is focussed on building endurance by means of increasing total miles per week and increasing long run distance, mostly at a modest pace.  The second mesocycle places the emphasis on developing capacity to handle lactate, by adding a fairly demanding weekly lactate threshold session.  The third mesocycle prepares for running at marathon pace, while also including some faster sessions that are likely to promote the development of type 2a fibres.  The fourth is a three week taper.  This program is for experienced runners, and provides a fairly demanding combination of high volume at moderate intensity, lactate threshold development, and a modest amount of faster running.


The program developed by the Furman Institute entails only three running sessions per week: an intense interval session, a tempo session and a long run at a demanding pace.  In addition, the athlete is encouraged to do a substantial amount of cross training.  The Furman Institute has demonstrated that their program can lead to impressive performances, even by relatively inexperienced athletes.  I think that this program is perhaps the most efficient way to produce the shift from the black line to the blue in figure 1.   However to my taste, it is a rather brutal program.  Furthermore, adequate  cross training to augment aerobic conditioning is crucial.


The most successful distance coach of the modern era is Renato Canova, who coaches several of the leading Kenyan half marathon and marathoners.  He places much less emphasis on  low intensity running and greater emphasis on long tempo runs.  The key sessions in his marathon program are long runs at a pace very near to marathon pace.  However, Canova’s athletes almost certainly commence their training with well developed capillaries and mitochondrial enzymes, based on years of running to and from school in many instances.


The key lesson to be gleaned for figure 1 and supported by a brief review of the training programs recommended by experienced coaches is that the optimum training for an individual depends not only on the target race, but also on experience and fitness at the start of the training block.  At present, I am preparing for a half-marathon, which therefore tips the balance a little towards higher intensity sessions compared with marathon training.  But, I started this current training block with a less well developed aerobic system than I would have wished.   So it remains unclear whether or not I have been wise to move from a predominantly low intensity program to a program including tempo runs, intervals and progressive long runs.  However if my ability to handle lactate is improving, I might nonetheless be nearer to optimum race-fitness despite not yet having achieved maximal aerobic development.  I am aware it is a gamble, but I think that if I am to achieve the best half marathon of which I am capable this year, this is the preferred strategy.

Ewen jokingly claims to have found a bookie who is prepared to offer odds of a mansion in Forrest (the poshest suburb of Canberra) against Ewen’s garden shed on the outcome of my attempt to better my M60 HM best, achieved 6 years ago.  I think these odds are not unreasonable.  I have advised Ewen to make sure he removes his lawn-mower from the garden shed in advance, but I will certainly do my best to secure a mansion for him in Forrest , near to his favourite training runs around Lake Burley Griffin and not too far from Mount Ainslie.


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