Posted: October 12, 2004

Athletics: An Exclusive Report On A World-Record Attempt Made In (Or About) The Year 2025

By Craig Sharp, Professor of Sports Science, Brunel University

Any look at "Sports science for the millennium" must consider the fact that by its nature, there are no major breakthroughs in sports science, such as vaccines and antibiotics in medicine, or the genetic code in biology, or atomic theory in physics, or the big-bang in cosmology. Sports science in general consists of constant refinements or improvements across a broad front; a front that includes training, tactics, techniques, skills, equipment, biomechanics, psychology, chronobiology, nutrition, management and physiology - as well as all the medical aspects. Thus, I have no dramatic breakthroughs to forecast, but instead I foresee continual improvement across the spectrum. Hence, I have written my view of a future scenario in terms of a world-record attempt to break the 24-minute 10,000 metres, set a few decades into the millennium.

Coe, the grandson
It was a special event. The attack on the world 10,000m record had been publicised worldwide, and the satellite sports channels had unique coverage. Steve Coe, the challenger, - grandson of a famous father, whose own world 800m record had lasted for almost as many years as Steve had been alive - had put in three periodised sessions daily for the past 24 months under his coach Harry Anderson, specifically to prepare for this attempt to be the first to run under 24 minutes for the distance. Luckily, or he would not have been attempting what he was about to do, Steve had been conceived with a genetic advantage in terms of his response to training. Athletes, otherwise equally endowed physiologically, may respond differently to the same training, because, as Professor Bouchard and colleagues discovered at Laval University, Quebec, some are genetically programmed to produce a better response to the same stimulus.

In carefully dovetailed micro-, meso-, and macrocycles Steve had put in hundreds of multiple daily sessions either on the indoor and outdoor tracks and courses, or on the computer-programmed Powerpace treadmill in his altitude chamber, complete with forced-draft wind simulation and projection screen with variable scenic or stadia video cassettes. Adinike, his sponsoring company, had developed a skintight hi-flo Lycra racing suit that both decreased wind resistance and increased heat dissipation, optimising heat loss both by not inhibiting radiation, and by optimally wicking sweat to the surface. It moulded his smoothly shaven head, and it maximised advertising space. Equally, he had undergone many hundreds of (precisely targeted) isokinetic and biokinetic conditioning sessions geared precisely to appropriate muscle groups at the shortening speeds to be expected at his racing pace. These muscle contraction speeds had been carefully worked out by biomechanical analysis.

Enhancing elastic energy storage
Even more importantly, Steve had placed a considerable training emphasis on plyometric lower-body work, to greatly enhance elastic energy storage in Achilles and other tendons, together with the ligaments of the transverse and horizontal arches of his feet. Decades before, R. McNeill Alexander of Leeds University had calculated that the elastic storage and return of energy in the Achilles tendon was some 35% of the energy of the running stride, while that of the foot ligaments was about 17%, i.e., over 50% of the energy in distance running was not generated metabolically. In those days, measures of VO2max and the OBLA point (onset of blood lactate accumulation) were thought to be the major determinants of aerobic fitness. That was mainly because there were then no measures of in vivo utilisation of such elastic energy, stored and released at every stride like a pogo stick. Now, with permanently inserted telemetry micro-strain gauges at selected sites, this important aspect of running economy could be monitored at will. Back in the 90's, Professor Carleton Cooke of Leeds Metropolitan University had discovered that elite marathon runners used some 5ml per kg per minute less oxygen running at the same speed as even good club runners. Yet his conventional biomechanical analyses of running style showed no obvious mechanical differences. One conclusion was that these efficient runners may have had a better return of elastic energy per stride.

About the same time, a report from Dr Gelim and orthopaedic collagues at Lenox Hill Hospital New York suggested that runners who were 'tighter' and less flexible, as assessed by 11 passive flexibility tests, might have better running economy than those who had greater joint mobility. Such relative slackness may have implied that the tendons were too long for their collagen to be optimally stretched - the pogo spring was too soft. However, Steve had been blessed with a skeleto-tendon system which was in excellent kinetic balance; moreover, genetically he responded far better than most to training. Thus, his Achilles energy return had been increased from 35% to about 45%, and that of his foot ligaments from about 17% to 20%. Thus 65% of the energy cost of each stride, (approx 85 Joules) at his racing speed, could be stored and returned, over 10% better than most.

Routine biomechanical and physiological assessments were performed as appropriate, although their usefulness latterly seemed to lie as much in helping his morale as in any new data which they brought him and Harry, unless there were any training breaks for illness or injury, which fortunately were short and seldom. Right at the start of his career, DNA profiling had indicated unusual clustering of what decades before had been discovered as "fitness genes", as reported in 1998 by Dr Hugh Montgomery and colleagues at the Rayne Institute in London. In addition, profiling of his mother's mitochondrial DNA had confirmed her unusually high abilities to process oxygen. The focus was initially on Steve's mother, herself an elite distance runner in her day, because mitochondria are the organelles in muscle responsible for the production of all aerobic energy, and all mitochondria are maternally derived. Knowing this, Steve occasionally reflected that the biblical Adam would not have been much of a distance runner, but presumably in the Garden of Eden there was little need to hunt and gather over long distances.

Sex, sleep and poetry
Over the past 30 months, Harry and Steve had embarked on a carefully selected racing programme at varying distances. But, life was not all racing and training. Steve had a steady relationship with his girlfriend, and they led a normal sex-life. This was beneficial, both psychologically and in terms of optimising his sleep patterns. Good sleep was considered important for maximising the natural growth hormone training-response, and the sex itself for raising androgen levels. Both sets of hormones had an anabolic effect in helping to optimise the muscle response to training stimuli. Breaks and short holidays were considered vital, as was reasonable intellectual stimulus in the form of music, drama, poetry and general conversation. For the same reason, Steve followed a fairly challenging set of distance learning courses.

Adinike had also developed a racing shoe weighing under 25 gm, with a sole incorporating the latest Pogothane insert, which not only increased foot-strike rebound by 22% without interfering with the natural connective tissue elasticity of his legs and feet, but also provided adequate plantar sensory feedback to minimise impact injury through the otherwise possibly false subjective estimation of comfort in the soles of his feet. The shoes also featured the latest micro-spikes. The Ariadne track, a highly advanced version of the old Harvard tuned track track, was programmed for Coe's body mass, stride length, heelstrike force and running cadence. The moveable roof for the Whizlet stadium would be electronically adjusted for perfect environmental control, and the master control for race pacing would be provided by the programmable light-guide "hare" built into the track kerb, and which his six pace-makers had been given a great deal of money and very strict orders to follow. The pace makers were not expected to stay with the race, but to trot round until their particular 3min 50sec four-lap section was called for.

Injections to minimise fatigue
Steve's weekly blood samples had been submitted to full automated analysis for cell counts and biochemistry, and his diet adjusted or supplemented where necessary, together with branched chain amino acid and endorphin injections into the cerebro-spinal canal (to minimise fatigue), routine intravenous glutamine (to increase lymphocyte nutrition and thus aid immune function), and slow-creatine with high carbohydrate (to enhance muscle energetics). Regular bone scans provided early warning of impending stress fractures, and nuclear magnetic resonance (NMR) scans for early inflammatory foci around tendon, ligament or the origins or insertions of muscle, were routinely performed.

Frequent and thorough clinical, physiotherapy, osteopathic, and podiatric investigations were performed to give further early warnings, and a sports masseur eased out the tired muscles twice every day. A nutritional biochemist, with the assistance of two dieticians, formulated most of Steve's food. His fluid replacement throughout had been geared to actual daily weight loss correlated with quantified NMR site-specific body fat estimations, and his electrolyte replacement was paralleled to the computed losses in sweat. Months of electronic stimulation, at 40hz square wave pulses on the respective motor points of carefully selected muscles, had optimised his functional slow and fast fibre-mix for the coming race; this had been preceeded by specific intramuscular injections of insulin-like growth factor (ILGF), to stimulate synthesis of the appropriate muscle proteins in the careful build-up phase of general conditioning.

Helping thermoregulation
Appropriate phases of contrasting 10hz stimulation had been applied over 96-hour sessions to maximise selected-muscle capillary beds, to increase local blood flow, in order to maximise the transport of oxygen and nutrients, and the removal not only of carbon dioxide and lactic acid, but also of heat. An important feature of Steve's physique was his light body weight which, at 57kg (just under 9 stone) gave him a very favourable skin surface area in relation to his body weight. The lighter the runner, the greater the proportional skin area. For example, an eight-year-old child weighing 25kg may have a skin area of .95 square metres; by 18, and weighing 70kg the skin area will be 1.80 square metres; i.e., the body weight may nearly have trebled, but the skin area has only doubled, so there is less skin per unit of weight. The smaller one is, the greater the relative skin area - and the greater the relative surface area available for heat removal, via radiation from the dilated hot skin blood vessels, and from the evaporation of sweat.

The distance runner needs a very large capillary micro-circulation in muscle, to flush the heat away in the blood, together with the large body surface area to release the heat into the atmosphere. To aid Steve's thermoregulation, the track was cooled, and throughout the run the stadium temperature at the level of the runners was kept at 15 deg C. This temperature reduction also increased the density of the air, which marginally increased the availability of oxygen, but aerodynamically also increased air resistance. These two factors offset each other, although the oxygen percentage was slightly augmented by the novel natural, rather than artificial, grass of the stadium.

Gene-specific triggers
Graded infusions of lactate over many months had helped raise Steve's anaerobic (OBLA) threshold much higher than could otherwise have been achieved. Such infusions had been controlled where necessary by similar infusions of sodium hydrogencarbonate, to adjust muscle pH, also monitored by NMR spectroscopy. Gene-specific triggers for enzyme-induction of hepatic and renal Cori-cycle enzymes had been injected in specific DNA-targeted virus vectors, to maximise that particular mode of lactate removal, whereby lactic acid is recycled in liver and kidney back to glucose and glycogen.

Steve had undergone many phased courses of post-hypnotic suggestion to minimise the subjective elements of fatigue, had practised regular mental rehearsal of incremental lap times and final time with the aid of a virtual reality simulator, and had been subjected to bouts of relaxation and autogenic training together with thought-stopping and biofeedback to counter stress and anxiety.

Boosting glycogen by 400%
In the final few days, major attention was paid to the most critical parameter of all, his muscle glycogen, as this was held to be the absolute key to success in the attempt. The optimum fibre-mix achieved by the nerve-doping, with the whole being boosted by site-specific slow-release insulin-like growth factor which had optimised his fibre-type profile together with the enzyme profile per fibre-type. This had set the scene for gene-programmed increase in muscle cell insulin receptors, together with the programmed synthesis of the glycogen-building enzyme glycogen synthetase and glucose transporter proteins. This all resulted in a glycogen boost up to 420 umol/g muscle, - over 400% of the normal resting level.

Over 400 umol of glycogen per gram of muscle was the minimal level value calculated (following the method of Oxford University Professor Eric Newsholme, who has run over 30 marathons), as necessary for a 24min race. However, the problem with so much glycolysis would be the resulting overwhelming production of pyruvic acid and its reduction to lactic acid. Specific mitochondrial-inducing training by the Swiss Hoppeler method had been carried out to maximise the lactate shuttle, whereby lactate would be oxidised to pyruvate mainly in Steve's upper-body slow muscle, and processed through Krebs' cycle to carbon dioxide and water. The extra carbon dioxide was welcome to maximise the respiratory drive, as a mild deficiency here could result in desaturation of haemoglobin, resulting in less oxygen reaching the working muscle fibres.

The reward? One billion pounds
Intra- and extra-cellular buffers had been optimised, mainly with the induction of the Newsholme-cycle of fast-hydrogencarbonate, by the process discovered by him well after his retirement, after the turn of the millennium. So the success of the entire enterprise depended upon whether, in his muscle fibres, Steve could produce enough glycolytic energy, yet still remove the resulting lactic acid protons fast enough, to sustain the pace of 25 consecutive 400m laps, each in 57.6s. In other words, what might at one time have been regarded as an aerobic event, now depended utterly on anaerobic factors. Great care had been taken to ensure that he had not been exposed in the previous 72 hours to any carbon monoxide (from car exhausts, although these were vastly lower than in 2000, and smoking had died out). Carbon monoxide turns haemoglobin into inactive carboxy-haemoglobin (COHb). Professor Peter Raven of Fort Worth had noted that COHb diminishes maximal oxygen uptake linearly. For example, 4% COHb, which used to be attained in a couple of hours of early millennium motorway driving, would diminish maximal oxygen uptake by 4%, which could significantly affect elite aerobic performance.

Dietary, electrolyte, fluid and psychological preparations were completed over the final 72 hours, with a final intravenous infusion of the fatigue-inhibitor antioxidant N-acetylcysteine (to which he was known not to react adversely) immediately before stepping out onto the track. Steve Coe had trained, peaked and tapered to the form of his life, and he was ready to run 10,000 metres in under 24 minutes before a mega-satellite 27-channel pay-sport audience of just over half the world. This would net him one billion pounds, and a lifetime of ease. (Acknowledgement: This represents an expanded, updated version of an article which originally appeared in 1996 in the British Journal of Sports Medicine, vol 30, pp181-182, published by BJM publishing group, who have kindly given permission for its use here.)

Appendix
The glycogen calculations for a sub-24 minute 10,000m are based on extrapolations from those of Professor Eric Newsholme of Oxford University:- 100m in 10s requires 3umol ATP per gram of muscle per second.

10,000 in 24min (1440s) = 14.40s per 100m. ATP needed is 3 x 10/14.40 = 2.08 umol ATP/g muscle/s Assume, for this 10,000m, that 65% ATP is provided aerobically and 35% anaerobically.

1) How much glycogen is consumed aerobically for this 10,000m?
2.08 x 65% = 1.352 umol ATP/g muscle/s = 1.352/37 = 0.0365 umol glycogen/g muscle/s [assuming 37 moles of ATP are produced per mole of glucose-from-glycogen] = 52.6 umol glycogen per gram of muscle for the whole race.

2) How much glycogen is consumed anaerobically for this 10,000m?
2.08 x 35% = 0.728 umol ATP/g muscle/s = 0.728/3 = 0.243 umol glycogen/g muscle/s [assuming 3 moles of ATP are produced per mole of glucose-from-glycogen] = 349.4 glycogen per gram of muscle for the whole race.

The total is 402 umol glycogen per gram of muscle, which is nearly four times the normal concentration of glycogen stored in muscle. (This compares with a 10,000m in 27min, during which 97% ATP might be considered to be provided aerobically, and 3% anaerobically, requiring, per gram of muscle, concentrations of 79 umol and 30 umol glycogen respectively; a total of 109 umol glycogen per gram of muscle, which is about the total amount of glycogen stored in 1g of muscle.)

Note: If the new Nobel prize-winning "chemiosmotic theory" data are used, whereby a fully oxidised mole of glucose is now thought to produce not 37 but only 31 moles of ATP, then the 24-min 10,000m would need 412 umol glycogen/g muscle, and the 27-min race 124umol/g.

References

Alexander, R McNeill. 1992.
The Human Machine.
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Cooke, C.B. 1990.
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PhD Thesis, University of Birmingham. Gleim, G.M., Stachenfield, N.S., Nicholas, J.A. 1990.
"The influence of flexibility on the economy of walking and jogging."
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Montgomery, H. et al.
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1998 Nature: 393, No 6682, p221.

Newsholme, E.A., Bloomstrand, E., Eckblom, B. 1992.
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Raven, P.B. 1987.
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Simoneau, J.A., Lortie, G., Boulay, M.R., Marcotte, M., Thibault, M.C., Bouchard, C.
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Physical activity science laboratory, Laval University, Ste-Foy, Quebec, Canada G1K 7P4.