Archive for May, 2010

Why do marathon runners have skinny legs, and should they do HIIT?

May 30, 2010

While trawling the web for a spectrum of opinions about the role of hormones in producing the effects of training, I came across a website with the title ‘’ [1].  The name of the site suggests dedication to the more fragile aspects of the male ego.  This impression was re-enforced by the proclamation:  ‘A picture is worth a thousand words, so I’m going to show you two right now.  First, take a look at this Olympic sprinter…’ [accompanied by a picture of a British sprinter who reminds me of a bison.]  ‘Now, compare him with this Olympic marathon runner….’ [accompanied a picture of a Finnish marathoner with slender gazelle-like legs].  The author of the web-page asks rhetorically ‘Need I say more?’ 

I suspect that my response to the implied question about which of the two physiques is more appealing differs from that of Mark Wilson, the web-page author.  Nonetheless, the site raises a very interesting issue.   Despite the pop-up adverts for testosterone boosting supplements, Wilson’s message is that exercise in the best way to achieve the desired physique, and his preferred approach is High Intensity Interval Training.   Wilson claims: ‘High intensity exercises are so good at reducing fat, building muscle, and increasing testosterone levels, that every male on planet earth should be doing them.’

High Intensity Interval Training (HIIT)

I have for some time been fascinated by HIIT, not because of the claims that it builds muscle (or even on account of its potential for increasing testosterone), but on account of the evidence that it increases aerobic fitness.   In fact, there is evidence suggesting that HIIT is more effective in increasing  aerobic fitness than in producing muscle hypertrophy.  In a series of experiments, Martin Gibala and colleagues at McMaster University in Ontario, Canada, have shown that low volume sprint interval training produces increases in muscle oxidative capacity similar to that produced by much higher volumes of conventional endurance training [2,3].  

For example, in one of the studies [3], ten healthy young men and 10 healthy young women were randomly assigned to either sprint interval training (HIIT) or conventional endurance training for a period of 6 weeks.  The HIIT consisted of four to six repetitions of 30 seconds of all-out sprinting on a cycle ergometer with a mean power output of around 500 watts, and 4.5 min of recovery between effort epochs, 3 times per week. The endurance training consisted of 40 to 60 minutes of continuous cycling at 65% of VO2max (mean power output of 150 watts) 5 days per week.   Training volume was 225 kJoules per week for HIIT and 2250 kJoules per week for endurance training.  Muscle biopsy revealed that both training protocols produced significant but similar increases in the mitochondrial enzymes responsible for oxidation of carbohydrate and of fats.  Thus, despite the 10-fold difference in training volume, HIIT  produced similar metabolic adaptations to those produced by endurance training.   How can this be?

The molecular mechanisms of training

Muscle is one of the most adaptable of human tissues and the past decade has seen spectacular increase in our knowledge about the physiological mechanisms by which training can improve muscle performance.  One might hope that this explosion of knowledge would provide rational answers to questions such as: why does HIIT increase aerobic capacity; what is the best training regime to maximize my performance in the marathon, or alternatively, in a 100 metre race; or even narcissistic questions such as how can I look ‘cut’ (which I think means looking like a heroic figure from a Michelangelo painting); or pragmatic questions such as how can I ensure I am still mobile when I am ninety.   But the reality is that despite a wealth of knowledge about mechanisms by which muscles respond to training, maximizing muscle performance is still an art as much as a science.  Nonetheless, it would be foolish to ignore the science because with current knowledge, the science can make a useful contribution and the best approach is almost certainly to integrate the art with the science.

There are two main classes of mechanism by which muscle performance can be improved: on the one hand, hypertrophy – which is probably important for maximizing 100m performance; is definitely essential if you want to look like a heroic figure from a Michelangelo painting, and might also help you remain mobile at age ninety; and on the other hand, an increase in oxidative capacity, which is crucial for running any distance from 800m to a marathon and beyond.  Current knowledge of muscle physiology provides useful guidance about the optimum strategies for producing either hypertrophy or oxidative capacity, though the question of how to optimize both simultaneously remains a vexed question. 

Cell signaling

The key scientific information is knowledge about mechanisms of cell signaling: the mechanisms by which ‘signals’ initiated by chemical changes such as depletion of the high-energy molecule ATP, or physical effects such as stretching of a muscle, lead to a cascade of chemical reactions that ultimately result in expressing the information coded in our DNA so as to produce proteins that enhance the function of our muscles.  Different types of training produce different signals which in turn produce different adaptations in muscle.  In particular, some signals lead to enhanced production of the proteins such as actin and myosin that form the contractile machinery of muscle cells.  These signals produce increase in strength and muscle diameter.  Other signals lead to enhanced production of the enzymes responsible for energy metabolism; in particular, the group of enzymes within mitochondria that form the cytochrome oxidase complex, responsible for oxidation of carbohydrates and fats.  

Some of us might be endowed with a genetic message that codes for proteins that perform their role more efficiently, and that might determine whether or not we become an Olympian or a recreational athlete, but whatever the fine details of the genetic message, our goal is to maximize our performance by adjusting our training schedule to optimize the expression of our own genetic information to produce the proteins that govern muscle performance.

The AMPK – PKB switch

In a key set of experiments in isolated animal muscles, John Atherton and colleagues from Nottingham University demonstrated that stimulation by prolonged low-frequency bursts of electrical stimuli, intended to mimic endurance training, activated signaling pathways  associated with development of mitochondrial oxidative capacity, while short, high frequency bursts, to mimic resistance training, activated signaling pathways associated with muscle hypertrophy [4].  

[A note about signaling jargon: Unfortunately the full names of the molecules in the signaling pathways are long, complex and utterly meaningless unless you have a detailed knowledge of biochemistry.  For convenience, scientists invent names based on the initial letters of the full chemical names – sometime producing whimsical but memorable labels like FOX but in other instance producing strings of initials that are incomprehensible jargon.  Fortunately, the tags assigned to the more important signaling molecules eventually become familiar and can be meaningful even without knowledge of the full name.  The initial signaling molecule in the mitochondrial oxidative pathway studied by Atherton is adenosine mono-phosphate (AMP) – a close relative of the high-energy molecule adenosine tri-phosphate (ATP).  The first step in the signaling pathway involves adding a phosphate group.  Enzymes that add phosphate groups are called kinases, so the name given to the signaling pathway the leads to increased mitochondrial oxidative capacity in the AMPK pathway, where the K refers to kinase.  Similarly the first step in the pathway that leads to muscle hypertophy is the addition of a phosphate group to a protein, carried out by an enzyme known as protein kinase B, so that signaling pathway is known as the PKB pathway.]

The observation that stimulation of the muscles mimicking endurance training led to increased mitochondrial oxidative capacity while stimulation mimicking resistance training resulted in increased signaling in the pathway to hypertrophy led Atherton and colleagues to hypothesize that the response of a muscle to exercise is determined by an ‘AMPK –PKB’ switch that determines whether or not the adaptation will be mainly increased oxidative capacity or hypertrophy.   This hypothesis would suggest that marathon runners have skinny legs because conventional endurance training throws the switch to activate the AMPK pathway.  Broadly speaking, the evidence supports this notion, though as we shall see, the picture is more complex.

The molecular mechanism of HIIT

A key player in the cascade of reactions that leads to increased mitochondrial oxidative capacity is a protein with the memory-boggling name:  Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (abbreviated to PGC-1a).  This can be activated by a number of different signals including the AMPK pathway.  Giballa and colleagues have demonstrated that HIIT activates AMPK signaling leading to an increase in  the expression of PGC-1a in human skeletal muscle [5,6].   Thus, there is fairly clear evidence HIIT is an effective way to increase the oxidative capacity of muscle, and the signaling pathway has a crucial overlap with the signaling pathway involved in more conventional forms of endurance training.

As the evidence for the molecular mechanism of HIIT has emerged, it has become clear that it is potentially sensible for a marathon runner to include HIIT within his or her training program.  Of course one might say that Lydiard or Hudson reached similar conclusions without the need for complex science.  However, it seems to me that it is only by a combination of practical observation of what works, together with an understanding of the mechanism of why it works, that we will be able to make a rational choice between the competing claims of advocates of various different approaches to training.  As for the claim  on the ‘’ website that ‘High intensity exercises are so good at reducing fat, building muscle, and increasing testosterone levels, that every male on planet earth should be doing them.’, the evidence from the studies by Gibala does not disprove this claim, but it does suggest that one of the major consequences of HIIT is switching on the signaling path that leads to increased aerobic capacity, similar to the outcome of endurance training programs that produce skinny-legged marathon runners.  If my only goal was muscle hypertrophy, I would place more emphasis on weight training than on HIIT.  On the other hand, if my goal is to produce strong but skinny legs, I would definitely include HIIT in the program.

But other things have to be considered

The studies by Martin Gibala and his colleagues suggest that HIIT might be the most time-efficient way to improve aerobic capacity, but despite being a crucial goal of training for distance running, improved aerobic capacity is not the only goal.  For the long distance runner, even more crucial is the need to develop resistance against fatigue.  HIIT is likely to produce its greatest effects on type 2A (aerobic fast twitch fibres) but these are less fatigu- resistant than type 1 (slow twitch fibres).  It is likely that type 1 fibres can be developed more effectively by more sustained less intense training.  Nonetheless, for distance extending from 400m to the marathon, peak performances requires highly developed type 2A fibres as well as type 1 fibres, and it is worthwhile devoting at a portion of one’s training program to developing the type 2A fibres. 

Among many other requirements is the need to develop the strength and resilience of muscles and other connective tissues, to avoid injury.  There is indeed reason to believe that HIIT might also help develop these capacities.   If HIIT takes a form similar to the wind sprints advocated by Arthur Lydiard, or the short hill sprints as advocated by Brad Hudson, it is likely to be effective not only in enhancing aerobic capacity but also in developing the strength and resilience of connective tissues necessary to minimize risk of injury, and also in developing good neuromuscular coordination.

The studies of Gibala do not address the question of how HIIT might be integrated into a higher volume training program. Lydiard included wind sprints in sessions that also included long hills, but my own experience suggest that this detracts from the ability to exert full effort during the sprint, and it is possible that the increased level of stress hormones such as cortisol might impede the anabolic benefits of the HIIT.  I am more inclined towards Brad Hudson’s approach.  He recommends performing short hill sprints on easy days      

Signaling via Nur77

Also important is the ability to utilize fats while conserving glucose.  It is probable that another signaling mechanism involving the nuclear hormone receptor, nur77, plays an important role in this.  Nur77 regulates the expression of genes involved in lipid metabolism and in the storage, release and transport of glucose into cells.  Nur77 signaling is activated by exercise and other stressors.    A recent study by Lewis and colleagues from Harvard University [7] has demonstrated that fit athletes can be distinguished from less fit athletes on the basis of blood levels of various metabolites that interact with nur77.  It is probably that high levels signaling via nur77 result in efficient mobilization of lipids.

Nur77 also plays a key role in the processes of inflammation.  As mentioned in my recent posts, acute inflammation appears to play a role in mediating the beneficial effects of training, but chronic inflammation may be a key factor in over-training and possibly also in long term tissue damage, leading to muscle wasting and perhaps to heart damage.  I will return to consider this important issue in more detail in the near future.


Recent advances in understanding cell signaling open up the vista of a world in which it might be possible to plan training programs that optimize the chance of achieving specific goals taking account of both our individual circumstances and our genetic make-up.  However the complexity of the emerging picture makes it clear that for the time being, training remains an art as much as a science.  Nonetheless what we do know of the science is enough to allow us to understand why different training programs produce different results, and also provides some clues as to how a training program might be tailored to meet the specific needs of an individual athlete.   In particular, the evidence suggests that inclusion of HIIT in a distance runner’s program is likely to result in strong, skinny legs.



[2] Gibala, M.J., Little, J.P., van Essen, M., Wilkin, G.P., Burgomaster,K.A., Safdar, A., et al. 2006. Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance. J. Physiol. 575: 901–911. doi:10.1113/jphysiol.2006.112094. PMID:16825308.

[3] Burgomaster, K.A., Howarth, K.R., Phillips, S.M., Rakobowchuk, M., Macdonald, M.J., McGee, S.L., and Gibala, M.J. 2008. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. J. Physiol. 586: 151–160. doi:10.1113/jphysiol.2007.142109.

[4] Atherton, P.J., Babraj, J., Smith, K., Singh, J., Rennie, M.J., and Wackerhage, H. 2005. Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB J. 19: 786–788.

[5] Gibala, M.J., McGee, S.L., Garnham, A.P., Howlett, K.F., Snow, R.J., and Hargreaves, M. 2009. Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1a in human skeletal muscle. J. Appl. Physiol. 106: 929–934. doi:10.1152/japplphysiol.90880.2008.

[6] Gibala, M.J., and McGee, S. 2008. Metabolic adaptations to short term high-intensity interval training: a little pain for a lot of gain? Exerc. Sport Sci. Rev. 36: 58–63. doi:10.1097/JES.0b013e318168ec1f. PMID:18362686.

[7] Lewis GD, Farrel L,  Wood MJ et al  2010 Metabolic Signatures of Exercise in Human Plasma Science Translational  Medicine, 2 (Issue 33),  33 – 37

Training, recovery, sleep and growth hormone

May 9, 2010

Training produces tissue damage and improved fitness is the result of the way the body compensates for that damage.  This simple fact implies that promoting effective compensation is at least as important as the training itself.  Yet much of our attention in planning a training program is directed at determining how we can adjust the content of our training achieve the maximum tissue damage and yet still recover.  Most of us devote less attention to optimizing the process of recovery. 

Usually our body reminds us we need to re-hydrate, and we would be foolish to ignore that need.  Some of us give thought to post-training nutrition, and many dietitians recommend strategies such as consuming carbohydrate and protein in the ratio of 3:1  or 4:1 but the scientific evidence supporting such strategies is controversial.  Similarly some of us engage in post-run stretching but there is less convincing evidence that post-run stretching makes a great deal of difference.  Perhaps those of us with time and money get a regular post-exercise massage but there even less evidence that this leads to improved performance.  I do not discount the possible value of any of these post-run rituals – nutrition, stretching or massage – but on the whole, as far as I am aware, the quality of the evidence for their benefit is relatively limited.

What do Africans do?

In the absence of good scientific evidence, perhaps the most sensible approach is to look at what successful athletes do.  In my post on 27 April ‘How fast should the long run be’, I quoted from a magazine article by Hilary Stellingwerff, a Canadian runner who had spent some time training in Ethiopia at the invitation of Haile Gebrselassie.  She said:  “Athletics comes number one for African athletes; there is nothing else. They train very hard and sleep the rest of the day to recover.’ [1].  Plentiful sleep also features in the recovery strategy of Paula Radcliffe.  In an interview with Rachel Cooke for Observer Sport Monthly several years ago, she made it clear that, like the Africans, she spends a lot of time sleeping.  ‘I’m usually in bed by ten and I don’t get up until around nine,’ Paula reports. ‘Then I have another two hours sleep in the afternoon. You really need that sleep when you train as hard as I do.’  [2]

What does science tell us?

There is in fact a small amount of scientific evidence supporting the hypothesis that extra sleep improves athletic performance.  Cheri Mah and colleagues at Stanford University carried out a study in which 6 basket-ball players from the Stanford team maintained their typical sleep-wake patterns for a two-week baseline followed by a period in which they obtained as much extra sleep as possible. Significant improvements in athletic performance, including faster sprint time and increased free-throws, were observed [3].  

It is likely that one of the major physiological process by which sleep promotes recovery is the release of growth hormone.  Growth hormone is an anabolic hormone that is released from the pituitary gland in a pulsatile manner, typically in four of five bursts per 24 hours.  The most substantial burst occurs during the first two hours of sleep, though several smaller pulses are released at later stages during sleep.  A young adult typically secretes a total of around 400 micrograms (0.4 mg) per day.

Many features of the physiology of growth hormone relevant to runners were discussed in a  review by Widdowson and colleagues [4].  Growth hormone promotes the mobilization of fatty acids and would be expected to promote the use of fat as fuel when running.  Exercise itself, especially anaerobic exercise and resistance training, promotes the release of growth hormone.  In the context of recovery, the most relevant of the many actions of growth hormone is the promotion of muscle development. 

Does additional GH enhance performance?

The evidence for beneficial effect of injections growth hormone on athletic performance has hitherto been equivocal, but a recent large and rigorous study by Ken Ho and colleagues at St Vincent’s Hospital in Sydney, funded by the World Anti-doping Agency, has provided striking evidence of benefit, though also an indication of some risks [5].  96 healthy, young recreational athletes (average age of 27) took part in the eight week study. The 63 male athletes were randomly assigned to one of four regimens: 2 mg per day of growth hormone (about 5 times the amount typically released daily from the pituitary in young adults); 250 milligrams per week of testosterone; both growth hormone and testosterone; or placebo injections. The 33 female athletes received either growth hormone (2 mg) or placebo injections.   The allocation to treatment groups was double blind so neither the athletes nor the investigators knew who was receiving hormones and who was receiving the placebo.

After eight weeks, sprint capacity had shown an improvement that was 3.9% greater in the group receiving growth hormone than in the group receiving placebo injections.  A 3.9% improvement would reduce a 100 metre sprint time of 10 seconds to 9.61 seconds, enough to convert an ‘also ran’ to a medal winner in many races.  The male athletes who received both growth hormone and testosterone had an 8.3% average increase in sprint capacity.   However the sprinting performance returned to normal six weeks after the growth hormone injections stopped. Somewhat surprisingly, the improved sprint performances were not accompanied by increased strength or power.

Consistent with the known effect of growth hormone on fat metabolism, growth hormone reduced body fat and increased lean body mass.  However, consistent with the observation of the adverse effects in the disorder, acromegaly, in which the pituitary gland produces excessive growth hormone, the athletes receiving growth hormone also reported swelling and joint pain.   On balance this study by Ho and colleagues demonstrates that the World Anti-doping Agency should put more effort into testing for abuse of growth hormone.  From the perspective of the athlete who wishes to optimize both performance and health, the evident conclusion is that optimizing natural release of growth hormone release is likely to be worthwhile.  So perhaps the focus on sleep in the recovery stagy of both Paula Radcliffe and the African runners described by Hilary Stellingwerff appears very sound. 

There is only the fragmentary evidence such as that from the study by Cheri Mah at Stanford that increasing sleep might produce a large enough increase in growth hormone to affect athletic performance.  However, our understanding of the nature of the training effect suggests that when an athlete has reached a plateau where performance no longer improves despite regular training, perhaps the most rational approach is to devote at least as much attention to facilitating recovery as to adjusting the content of training sessions.  Getting enough sleep might well be the best place to start.


[1] Hilary Stellingwerff   ‘Living the High Life.’  Canadian Runner, Issue 2.4, 2009.

[2] Rachel Cooke   ‘In it for the long run’ Observer Sport Monthly, Sunday 1 December, 2002.  (,,849746,00.html)

[3] Mah C . presented at SLEEP 2007, the 21st Annual Meeting of the Associated Professional Sleep Societies (APSS). (Reported in: American Academy of Sleep Medicine. ‘Extra Sleep Improves Athletes’ Performance.’ ScienceDaily, June  2007)

[4] Widdowson WM, Healy M-L, Sonksen PH, and Gibney J.  The physiology of growth hormone and sport.  Growth Hormone & IGF Research 19 308–319, 2009

[5] Meinhardt U, Nelson AE, Hansen JL, Birzniece V, Clifford D, Leung K-C, Graham K, and Ho KYY. The Effects of Growth Hormone on Body Composition and Physical Performance in Recreational Athletes: A Randomized Trial.  Annals of Internal Medicine, 152 (9): 568-577, 2010.

The Mind of the Marathon Runner: London 2010

May 5, 2010

Why was the men’s marathon in London 2010 such a damp squib? The field was one of the strongest assembled for a big city marathon, and the weather, though a little humid, was fairly good for marathon running.  But Tsegaye Kebede was on his own for the last 8 km and the winning margin was 64 seconds.

Not only did the field include the formidable trio of Kenyans, Samuel Wanjiru, gold medalist from Beijing; Abel Kirui current world marathon champion; and Duncan Kibet, the second fastest marathon runner in history with a time of 2:04:27, but also Zersenay Tadese from Ethiopia, who had set a stunning world record in the half marathon in Lisbon five weeks earlier, though he had yet to complete an international marathon; Emmanuel Mutai, second placed between Kirui and Kebede in the world championship in Berlin in 2009; and Jouad Gharib, third in London in 2009.

Despite the fact that Wanjiru had suffered disruptions to his training due to injury in January and had expressed some doubts about the outcome for the race in a pre-race interview, as described in the discussion with Ewen following my posting on 27th April, the strength and depth of the field still appeared to promise a tightly fought finish. This seemed even more likely when a large leading group reached the half way point in a time slower than 63 minutes. 

Then shortly after halfway Mutai increased the pace dramatically, and only Kirui and Kebede were able to stay with him.  By 30 Km, Mutai had dropped back.  Nonetheless, for a few Km it looked as if the ‘end game’ might be a great duel between Kirui and Kebede.  But suddenly Kirui was no longer there.  Unfortunately, on account of the greater interest of the BBC in the women’s race, especially in British hope, Mara Yamauchi, the cameras did not record the moment when Kebede made the decisive break, but for the final 8 Km he had the race to himself, crossing the line in 2:05.19.  Mutai had moved forward again to second place in 2:06.23, and Jouad Gharib was third yet again, in 2:06:55, while Kirui had dropped back to fifth place, and Tadese was seventh, almost 7 minutes behind Kebede.  Wanjiru and Kibet had dropped out.

It is probable that various factors confounded the hopes for a hard fought race to the line.  One possible factor was the disruption of air travel due to the ash from the Icelandic volcano.  This undoubtedly caused a serious problem for Mara Yamauchi, who was forced to make a complex 6 day journey from her home in Japan.  While one can have sympathy with Mara, travel disruption appears a less credible excuse for the elite men, who were airlifted to London by private jet hired by the London marathon organizers at considerable expense.  So what might have been the main factors?

Mind and brain

Two scientific studies add to the growing evidence that the determinants of athletic performance are far more complex that the physiological aspects of physical fitness, such as oxidative capacity of muscles, muscular strength or cardiac output. 

A recent study by Macora and Staiano from Bangor University provided a graphic illustration of the influence of mental evaluation of the task ahead [1].  In the first stage, a group of fit young men cycled on a stationary bike at 90% of VO2max (an average power output of 242 watts) until the point of exhaustion; the point at which they could no longer maintain that power output.  This point was reached typically after about 10 minutes.  The participants were then required to attempt immediately to produce the maximum power output possible in a five second burst.  The peak power achieved during this five second burst was 731 watts, which is more than three times as large as the power output during the sustained test to exhaustion.  This clearly documents the fact that our mind sets limits on the power output our body can achieve, according to the expected duration of the demand for effort.

Even more recently, a study by Gant and colleagues from Auckland University  has demonstrated that sensory stimuli which trigger an expectation of a fresh supply of fuel can act via the brain to increase the power of muscle contraction [2].   Swilling a carbohydrate rich mixture in the mouth without swallowing produced an increase in muscle power not observed after swilling a similar tasting drink without carbohydrate.    Furthermore, the increase in muscle power associated with the carbohydrate-rich drink was accompanied by an increase in brain activity in the part of the cerebral cortex that controls muscle contraction, demonstrating that the effect was mediated by the brain.

What both of these studies show is that signals from the brain set the limit on power output, and these signals can be adjusted by both conscious and non-conscious mechanisms.  The crucial question that these studies raise is : how much can we train the brain to increase power output when it is most needed?  Athletic training largely focuses on developing peripheral physiological capacities such as blood supply to muscles and cytochrome levels in mitochondria.  However, perhaps more attention should be paid to training the central nervous system.

Competitive middle and long distance runners fall into two categories: aggressive front runners and those with a strong finishing kick.   In part, natural physical endowment plays a role in determine which type of runner you might be, but training and mental preparation are also crucial.   Perhaps the most famous aggressive front runner was Steve Prefontaine who cultivated the mental toughness to crush his opponent by setting a murderous pace from the start.  However, perhaps because of my Australian roots, I think I have learned more through pondering three famous athletic duels, each with an Australian link.

Landy and Bannister

My early memory of sport are dominated by the challenge of the 4-minute mile.  Like many young Australians at the time, all my hopes were invested in John Landy.  In the early 1950’s I loved running, though my own involvement was entirely non-competitive.  I simply enjoyed running to and from school.  As the years went by, I looked forward to the day when I would be able to run in the mile on sports day at school, but I never dreamt that I would actually win a schoolboy mile state championship one day.  To be realistic, my lack of dreams on my own behalf was well founded.  I only won that schoolboy championship race because atrocious weather and a water-logged grass track converted the mile into an endurance event, well suited to my preparation based on running to and from school.  While my lack of dreams of glory for myself were well founded, it was almost unthinkable that Landy would not be the first to run a mile in less than 4 minutes. 

It was era when the world’s first commercial jet airliner, the De Havilland Comet was famous for crashing, and the piston-engined Lockheed Constellation with its elegant dolphin shaped fuselage and three finned tail, was on the verge of obsolescence.  International sportsmen often traveled by ship.  As a result we were far less aware of the leading European or American athletes, such as Roger Banister or Wes Santee. Landy filled  the foreground of our awareness.  In the antipodean summer of 1953-54 Landy recorded 4:02.x on four occasions, and then set out for Europe where he would renew his attempts in the European summer, pushed by stronger competition.  When we heard that Oxford medical student, Roger Bannister had broken the 4 minute barrier in May, assisted by his pace-making friends in an event at Iffley Rd, it seemed such an anti-climax.  In June, Landy snatched back the world record with a time of 3:57.9 at Turku in Finalnd.  However the real battle would occur in August 1954 when Landy and Bannister lined up for the mile at the Empire Games in Vancouver.      

As a runner who had done much of his racing far from the more competitive environments of Europe and America, Landy had relatively little experience in tactical running.  In contrast, Bannister had honed his legendary final kick with scientific precision in sessions with his friends Chris Brasher and Chris Chataway   In that miracle mile in Vancouver, Landy decided his best strategy was to establish a good lead by the end of lap three, and was about 10 yards ahead at the bell.  However the crucial moment occurred as the runners came off the final bend and into the home straight.  Landy looked over his left shoulder as Bannister stormed past on his right.  Bannister won in 3:58.8, though both runners recorded a time under 4 minutes. 

Bannister and Landy were both men of outstanding character.  Landy will be long remembered by his compatriots not only for his herculean attempts to break the 4 minute barrier, but also for magnanimously stopping to assist Ron Clark  when he fell during the 1500m final at the Australian National Championships in 1956.  Landy went on to win the race.   Landy achieved a lifetime PB for the mile almost a second faster than Bannister, but Bannister quite deservedly has a much more secure place among the running greats, and he emerged as the victor in that dramatic head-to-head contest, largely because of Landy’s momentary loss of confidence coming into the home straight.  

Pirie and Kuts

In 1956, the international tensions of the deepening Cold War were exacerbated when Russian tanks had rolled into Budapest to crush the Hungarian revolution.  However, the dominant event looming in the minds of many Australians was the Melbourne Olympics.  By this time, Emil Zatopek, triple gold medalist in Helsinki four years previously, was fading and the dominant figures in 5000m and 10000m were Valdimir Kuts from Russia, Sandor Iharos from Hungary and the Englishman, Gordon Pirie.    Kuts, a Red army officer with an aggressive front running style, had captured Zatopek’s 5,000m world record 1954.  In 1955, Sandor Iharos snatched that record from Kuts.  Then in June 1956, in Bergen, Norway, Gordon Pirie achieved a convincing victory over Kuts, while taking possession of the world record with time of 13:56.8.    In 1954 Zatopek’s record for the 10,000m had fallen to Iharos.   The Hungarian held it until Kuts took it in a race in Moscow shortly before the Games with a time of 28:30.4. 

Unfortunately Iharos’ career disintegrated in the turmoil following the Hungarian revolution, and the expectation for Melbourne was a battle between Kuts and Pirie, certainly in the 5,000m and perhaps also in the 10,000m.  Pirie had established his supremacy over Kuts in the 5,000m in Bergen, but Kuts arrived in Melbourne in great condition, fresh from his 10,000m record-breaking run in Moscow.  However Pirie also took pride in his gritty endurance based on prodigious volume of training, much of it at high intensity.  He ran over 200 miles per week.  His coach was the ‘father of interval training’, Woldemar Gerschler.   It is probable that in Pirie’s mind he nurtured the belief that he could crush Kuts in the 10,000m as well as the 5,000m. 

This was not going to be an amateur contest such as we had seen in Vancouver two years before between a privileged Oxford medical student and a gentlemanly Australian.  In the fifties that adjective didn’t seem such an oxymoron – in those days amateur athletics cultivated an Arthurian aura of honour in Australia as in Britain.  But, in the Olympics we expected a ‘bare knuckle’ confrontation between a forthright non-establishment Englishman with an axe to grind, and a Russian army officer who appeared to embody the ruthlessness of a formidable monolithic state. 

The final of the 10,000m occurred first.   Both runners believed that they had the endurance and toughness to prevail in a long surge to the finish, and the pressure built up with Kuts setting the pace. With five laps to go, Pirie took the lead but a lap later, Kuts surged back,  Pirie cracked and Kuts held on to take the gold medal in an Olympic record time of 28:45.6.  Pirie struggled to the finish in eighth place, 64 seconds behind Kuts.  In the 5,000m, the memory of Bergen had been replaced by the raw experience of the battle for mental supremacy a few days earlier, and Kuts again took the gold with Pirie trailing 11 seconds behind him in second place.      

As an incidental footnote to the international tensions of 1956, after the infamous ‘blood in the water’ polo match between Hungary and Russia, it was in Melbourne that the tradition of athletes from different nations mingling with goodwill during the closing ceremony of the Games was introduced, replacing the previous tradition of marching in ranks behind national flags.

Tergat and Gebrselassie

Forty-four years later, the Olympics returned to Australia, this time to Sydney.  I too returned to Australia that year, not on account of the Games but to visit my dying father.  In the intervening years I had too been a medical student at Oxford and had experienced a frisson of excitement running on the Iffley Road cinder track where Bannister had run the first sub-4 minute mile.  But by 2000, I was overweight and unfit.  I was now living in Vancouver.  The old Empire stadium where Bannister had defeated Landy had long since been demolished, but, inspired by the forest trails of the Pacific Spirit Park, I was just beginning to run again.  Shortly after my arrival back in Adelaide, one afternoon I was assisting my elderly mother into a taxi outside the house where I had spent my childhood, on our way to visit my ill father in the Royal Adelaide Hospital, when my elder brother drove past.  He stopped the car about 150 yards down the road, and because it seemed the natural thing to do, I set off unthinkingly at a brisk trot along the road to greet him. As I returned to the cab, the driver grinned at me: ‘With a turn of speed like that, you should be in Sydney, mate.’   Although there were more serious things on my mind that day, that little incident has stuck in my memory. 

The centre of gravity of distance running had moved unequivocally to Africa.   From the midst of an astounding wealth of talent among Kenyans, Ethiopians and Moroccans,  two outstanding figures had emerged to dominate the 10,000m in the closing years of the century, Haile Gebrselassie of Ethiopia and Paul Tergat of Kenya.  Gebrselassie had set a world record of 26:43.53 at Hengalo in 1995, and after losing it, regaining it and losing it again, he had recaptured the record with a time of the on 26:22:75 in 1998, again at Hengalo.  In the intervening time, Tergat had been in possession of the record for almost a year, with a time of 26:27:85 run in Brussels in 1997. 

Although Gebrselassie arrived in Sydney in 2000 as the current world record holder, Tergat was currently in great form, having recorded a time of 27:03:87 in Brussels only a month before Sydney.   He was determined to reverse the finishing order in Atlanta in 1996, when Gebrselassie had narrowly defeated him.   However a review of other previous head-to-head confrontations suggested that Gebrselassie was usually able to call upon some extra reserve when needed.  In both the 1997 and 1999 world championships, Gebrselassie had taken the gold medal and Tergat the silver.

The race was utterly spectacular. A pack of three Kenyans and two Ethiopians loped away from the rest of the field. At the bell, Haile was in a commanding position in second place, with his compatriot Assefa Mezgebu at his side, but all five were running strongly.  Tergat knew of Haile’s capacity to mount a devastating final sprint, whereas most of Tergat’s previous victories over his rival had been cross country events requiring physical strength. It is probable that he was thinking that his best strategy was to launch a strong attack relatively early in the final lap in the hope that his strength would prevail.  It was certainly crucial that he should begin the final sprint before Haile.  250m from the finish, Tergat made his decisive move.  He burst clear of the leading pack by a margin about 1 ½  metres, with Haile in pursuit.  As they sprinted around the curve, Haile slowly narrowed the gap, but on entering the home straight the space between them was still almost a metre and Tergat continued to look strong.  In that heart-stopping final 100m both athletes sprinted with amazing power.  The gap was narrowing at a scarcely perceptible rate and it looked as if Tergat might just hold on to his slender lead.  Less than 10 metres from the line Haile drew level and Tergat showed a faint flicker of weakening.  He dipped towards the tape desperately, but Haile had crossed the line less than a tenth of a second ahead of him, in a time of 27:18.20.


All three vignettes were duels between two fairly evenly matched athletes at the peak of their powers.  In all three instances, the stronger athlete prevailed, but the excess strength was more mental than physical.   The margins were quite different: Tergat crossed the line 0.09 seconds behind Gebrselassie, whereas Pirie was 64 seconds behind Kuts.  While it is probable that Pirie and Kuts were a little less closely matched than Tergat and Gebrselassie, the principle factor accounting for the difference in margins was the fact that the decisive test for Pirie occurred four laps from the end, whereas the decisive test for Tergat occurred only about 4 metres from the line.  According to Wikipedia, Kuts subsequently reported that if Pirie had held on any longer in their titanic battle, he, Kuts, would have submitted [3].

But the key feature of all three vignettes was the crucial point at which the battle was lost.  Landy looked over his shoulder as he came of the final bend with 100 metres to run; Pirie cracked as he and Kuts surged at a ‘suicidal’ pace with 4 laps to go; and Tergat’s posture sagged in a desperate dip only a few metres from the tape.  While the crux can be more easily identified in the body language of the vanquished, the mental state of the victor was equally important.  Bannister had developed his devastating final kick in training with his colleagues, Chataway and Brasher. Kuts had developed the mental strength to sustain a murderous, potentially even suicidal pace, long before the final lap, as he developed his aggressive front-running style.  Gebrselassie had demonstrated repeatedly during the five years leading up to the turn of the millenium that he could always dig a little more deeply whenever required in the final lap of a 10,000m race, and as he followed the powerful figure of Paul Tergat down the home straight in that titanic battle in Sydney, somewhere in the recesses of his brain was the confidence that he had the power to prevail.

Back to London 2010

As the three medal winners from the 2009 world championship in Berlin applied the pressure that demolished the remainder of the elite field shortly after the halfway in London 10 days ago, there were few pointers as to which of the three would eventually be the victor.  Mutai, who had been second in Berlin,  had initiated the surge in London, but after about 8 Km, he apparently sensed that he was not as strong as his two rivals and dropped back, conserving his energy for a final effort that would secure second place here, as in Berlin.  Kirui had been victor in Berlin and had that memory to buttress his confidence.  Unfortunately due to BBC’s preoccupation with the women’s race, I do not know what tipped the balance in favour of Kebede.  Did he have the confidence to surge again, as Kuts had done to crush Pirie in the 10,000m final in Melbourne?  Whatever happened, Kirui, like Pirie fifty-four years previously, cracked, and eventually finished almost three minutes behind Kebede.

The race failed to provide the exciting finish promised by the strength and depth of the field assembled at the start, but in retrospect, the way in which various factors ranging from Wanjiru’s  pre-race loss of confidence due to injury in January; the vagaries of travel though the dust of a volcano cloud; and above all, the way in which the mental strengths of the three medal winners from the world championship in Berlin determined events in the second half, made London 2010 an event to contemplate and savour.  


[1] Macora and Staiano (2010) ‘The limit to exercise tolerance in humans: mind over muscle’ (Eur J Appl Physiol.. [Epub ahead of print])

[2] Gant et al (2010) Brain Research, DOI: 10.1016/j.brainres.2010.04.004