JUST ONE QUESTION . . . We all know that we are able to move bits of ourselves back and forth, up and down because, within themselves, our muscles generate the energy for us to do so. We presume that our training for running races will somehow provide us with bigger muscles, which will have greater power output so that we can go faster. So we split our training between first building up the relevant muscles and then maintaining that optimum size for the race we have foremost in mind to run well in.

Then, to provide the oxygen for "burning" the fat and carbohydrate which "fuel" that energy production, we need somehow to develop our hearts to pump twice or even four times as much blood with each beat than the average couch potato can.

That’s simple, then. There’s just one question which needs answering : exactly how does muscle grow?

. . . AND THE ANSWER IS, er, not known. There are several physiology textbooks in our household, the biggest of which is "Textbook of Medical Physiology", by American professors Arthur C. Guyton and John E. Hall. After a description of the effect of training – or lack of it – as in:

• "When the total mass of a muscle enlarges, this is called muscle hypertrophy. When it decreases, the process is called muscle atrophy. Virtually all muscle hypertrophy results from enlargement of the individual muscle fibres". Yes, that’s what we thought: muscles get bigger because they, er, get bigger. And they waste away when we stop training.
• "This usually occurs in response to contraction of a muscle at maximal or almost maximal force". i.e., the muscles get bigger with the more demanding training.
• "Hypertrophy occurs to a much greater extent when a muscle is simultaneously stretched during the contractile processes". Physiotherapists call those "eccentric contractions".
• "Only a few such strong contractions each day are required to cause almost maximum hypertrophy within 6 to 10 weeks". That’s surprisingly quick, isn’t it?

they don’t waste time speculating as to how this desirable end comes about. As in:

• "The manner in which forceful contraction leads to hypertrophy is not known". Oh !

Hoping for something more specific than that, I then turned to "Exercise Physiology" by another set of American professors, William McArdle, Frank Katch and Victor Katch:

• "Muscle remodelling in resistance training is a complex process … the specific exercise response is linked to the configuration of the exercise stimulus (e.g., frequency, intensity, volume and mode of training)".

Thus covering all the bases : "frequency" = at least ‘n’ times a week ; "intensity" = at a demanding pace ; "volume" = whatever you have time for ; and "mode of training" = road or trail, circuits in the gym, cross-training, etc, etc.

• "The two primary hormones involved in resistance training adaptations are testosterone and growth hormone. It appears that testosterone’s primary role is to augment the release of GH and to interact with the nervous system. These functions may be more important than any direct anabolic effect of testosterone per se".
• "Not all research, however, has demonstrated a direct GH response to resistance training. Perhaps there is a threshold of exercise intensity or length of training necessary to elicit a GH stimulatory response".

No training leads to muscle atrophy ; a little training just maintains what we have built up in the past ; training over some, unknown threshold level builds new muscle.

• "Data on women with regard to testosterone and GH secretion with resistance training are scarce". Not a lot known, it seems.
• "The few available studies suggest that women do not demonstrate an exercise-induced increase in testosterone or GH. It is hypothesised that because of this inhibited response women are unable to hypertrophy to the same extent as men, even with extreme overload training".

That may be because when the book was written in 1994, it was a couple of years before the sensitivity of the apparatus analysing hormone amounts was enhanced by 100 times.

• "Continued careful research is needed in this area". If anyone is interested, that is.

MEANWHILE, it would help if we could develop a working hypothesis, based on our own observations of ourselves, on which we can build a muscle-developing training programme.

We can all remember the agony of those first few weeks when we took up running, with legs so sore and stiff that it was difficult to walk for the next couple of days, let alone run. McArdle and the Katches reckon that that was due to:

• "minute tears in the muscle tissue itself, muscle spasms or overstretching and perhaps tearing of portions of the muscles’ connective tissue harness". They also say that:
• "eccentric muscular actions generally cause the greatest post-exercise discomfort" and that "downhill running (eccentric actions) caused moderate to severe delayed onset muscle soreness … [with] corresponding increases in the levels of creatine kinase (CK), the enzyme used commonly as a marker of muscle injury".

It is also regularly reported in the running mags that total body weight of the novice runner goes up in the first few weeks of training "as muscle, which is more dense than fat, builds up".

Simply stated, it seems to me that, taking all that lot together, the most likely reason for the [unknown] "manner in which forceful contraction leads to hypertrophy" is that it depends on our training vigorously enough to injure ourselves, albeit only slightly.

WHAT ABOUT THE HEART : surely its increase in strength and size doesn’t depend on our "injuring" it, does it? Yes, in a word, it does.

The heart is a complex pump and it is a muscle made up of lots of fibres, just like skeletal muscle is, except that they work differently in a heart. We know that training makes hearts bigger and stronger than untrained ones, sufficient at least to double the amount of blood pumped out each beat and hence to reduce our resting heart rates to half or less than those of untrained people.

To find out how it does it, we need to go back to Professors Guyton and Hall, as in:

• "A heart that is subjected to increased workload – but not so much excess load that it damages the heart – causes the heart muscle to increase in mass and contractile strength in the same way that heavy exercise causes skeletal muscles to hypertrophy. For instance, it is common for the hearts of marathon runners to be increased in mass by 50 to 75%. This allows the heart to pump much greater than usual amounts of blood, sometimes 50 to 100% more".

Moreover, when the blockage of blood supply to a small area of it causes a mild heart attack, they write that:

• "the muscle fibres in the centre of the area die. After a few days, most on the non-functional area of muscle becomes functional again or dies, one or the other. If the latter, the dead muscle tissue is gradually replaced by fibrous tissue. Finally, the normal areas of the heart gradually hypertrophy to compensate for the lost musculature. By these means, the heart recovers either partially or almost completely".

It is not difficult to suppose that it is our "heavy exercise" which causes minor damage to heart fibres, the repairing of which results in heart enlargement, hence to increased oxygen supply to leg muscles and, eventually, to those much sought after PBs.

We should stop short of overdoing it and suffering an actual heart attack, though.

RUNNING RESEARCH NEWS is an American monthly journal which predated "Peak Performance" here by several years. It is owned by, published by and largely written by a Dr Owen Anderson, who is also on the Editorial Board of PP. I used to take them both, but so many of Anderson’s articles are reprinted word for word in PP – but with colour for color, fibre for fiber, etc – that I have just have PP now. Basically both are commentaries on research papers found by literature-searches on the Internet.

Coming so soon after the many VSN non-researched papers by Black, Briscoe and Jones on the various merits/demerits of training distances/speed/weekly mileages etc, I was taken aback to read the headline to Anderson’s article in the March 2002 edition of Peak Performance. It read "The risks of going long : when the super-fit endurance athlete turns into a heart attack victim". It opened with:

• "About 1 in 50,000. If you run marathons or participate in other forms of exercise which lasts three hours or more, that’s your approximate risk of suffering an acute heart attack or sudden cardiac death during or within 24 hours of your effort".

Disregarding Dr Anderson’s problem of his being unable to distinguish between "after" and "because of" and his arguing from a particular instance to a general conclusion too often, I found the article quite interesting after his illogical, unscientific introduction.

The research paper which had sparked his interest was a study of 38 participants in the 1999 Tyrolean Otzaler Radmarathon, a cycle race covering 230km and with an altitude change of 5500m.

• "The cyclists were free of cardiovascular risk factors and they had no evidence of heart disease. The researchers checked their blood levels for cardiac troponin I [CT I], an enzyme which is the specific marker for heart muscle death [i.e. it is the equivalent of CK for skeletal muscle]. All the cyclists registered zero for CT I before the start of the Radmarathon, but it had increased in 13, 34% of them, by the finish of it."

Anderson then listed the "risk factors":

• Age. Being young was "bad" ;
• Race Time. Racing fast increased the risk : the highest post-race CT I level was detected in the winner of the race ;
• Pre-race Training Distance. The higher the overall training volume, the greater the chances of increased CT I after the race.

My take on those "scientific conclusions" is that, as I wrote in my last CC, "if you keep doing what you did, you’ll keep getting what you got". Or, in other words, those who train the harder, particularly the younger ones, tend to win races and, both in training and racing, they stress more of their heart fibres to breaking point than those who lose races.

IT’S HAPPENED BEFORE. According to the Austrians:

• "many of the cyclists probably experienced sub-clinical cardiac injury during the event and this was associated with the actual death of heart-muscle cells".

Anderson then writes:

• "the mechanism underlying such cardiac cell deaths is unknown" – shall we tell him !! – but goes on to say that "raised levels of CT I have been observed in 9% of Hawaii Ironman Triathlon finishers in one study and in 11% of finishers of an alpine cross-country marathon".

But there is no suggestion that this phenomenon which Anderson has discovered is commonplace, probably occurring every time we train really hard – be it short and fast, or long and slower – and particularly when racing (which your correspondent is on record saying is "the best form of training"). As Guyton and Hall say:

• "increased workload, but not so much excess load that it damages the heart, causes the heart muscle to increase in mass and contractile strength in the same way that heavy exercise causes skeletal muscles to hypertrophy" – so it is reasonable to presume that the mechanism by which hypertrophy of one type of muscle is achieved may be the same as it is for the other kind.

THE HEALTH WARNING. This analysis may also solve another little problem which I have mentioned in these columns from time to time. It is that heart rate monitor supplier Polar and several of the coaches writing schedules in the magazines scarcely ever deviate from the "220 minus your age is your maximum heart rate" formula or, if they do, it’s to "205 minus half your age" if you’re a veteran who has been running for years.

In one of the mags I get from the States, there were schedules recently for "A First Marathon" in which virtually all the short training sessions were to be at 60% of MHR and only the repeat, track miles and a few of the semi-long runs at 70% or 80%. I walk fast at 60% of 220 minus my age, I run 80% age-graded ½ marathons at my 100% MHR and I ran the Thirsk 10 this year at an average of 148bpm, which is 102% of my alleged maximum-to-exhaustion-on-a treadmill heart rate. Surely there must be some mistake?

Well, no, there isn’t actually, if my experience in the last six years of my with-pay employment in the Insurance industry is relevant. Crucial in product development and marketing in manufacturing industry is the concept known as Strict Liability, the central principle of which is that the responsibility for a product’s quality and its safety in operation is borne by the producer, not by the retailer or by the customer.

In the UK, the classic case which resulted in the 19^th century in the first Sale of Goods Act was that of the young lady who found a [dead] snail in a jar of pickles she had bought. Although technically her contract was with the retailer, it was the bottler who was judged to have been guilty of producing goods which were "not of merchantable quality".

Stories abound in the USA of producers of goods being taken to the cleaners by their customers, even those who acted unimaginably stupidly. One was the case of the woman who successfully sued the manufacturer for not telling her she would kill her pet poodle if she put it in the microwave to dry it after its bath. Another was that of the granny who spilt a carton of Macdonald’s coffee – which she alleged was too hot – and scalded her thigh when her daughter drove away too quickly from a Drive-In. And of the father who was throwing his young son up into the air and catching him, with peals of laughter all round, until he threw the lad a little too high and his head was cracked by a blade of the room’s air circulating fan. Its maker had to pay up for not having put a guard on the fan or for not having warned the father not to do that. Or both. I forget the details.

Hence, I guess, why the recommendations from the American author quoted above for the first time marathoner did not say "aim to run your fast tempo runs at around at pace which will get your heart up to 105% of its nominal rate of 220 – age and the marathon itself at around 98% [which was the average I registered the last time I ran the London marathon at over 80% age-graded]". If he had done so and one of his readers had died who happened to have been running with a bad cold or after he’d had a blazing row with his boss, then the family would surely have been awarded at least $10million in costs and punitive damages against the author of such a dangerous recommendation.

DISCLAIMER. It is probably too late already but I hereby proclaim that what may have seemed in Coach’s Columns in the last six years to have been recommendations from me to you to train at around a 220 minus your age heart rate and to race at 5bpm higher than that was actually merely my informing you that that is how I train and race now that I have had six years’ worth of experience of using a Polar heart rate monitor.

I trust that is quite clear, even though I’ve written it all in one sentence, of 82 words, without any punctuation, just like a proper lawyer does. O.K.!?

And recalling Owen Anderson's third point that "pre-race training distance : the higher the overall training volume, the greater the chances of increased CT I after the race" - Paul and George may wish to add their disclaimers, too !

Written after England vs Sweden and before England vs Argentina, unedited

Shortly after I had finished writing June's Coach’s Column, those sports watchers in the UK with a passing interest in Soccer were encouraged to believe that England’s young, inexperienced players would go far in the World Cup. A communiqué from Beckingham Palace revealed that King David’s broken left foot second metatarsal had healed and he would definitely lead the team on to the pitch for the first match against Sweden, a team England has not beaten since 1968.

Just hold on a minute. We know, even though the media pundits don’t, that the enforced inactivity caused by the injury would have led to a very considerable atrophy of skeletal and heart muscle fibres. Although we can suppose that the Man United and England physios will have reduced that loss by working on Beckham’s lower limbs for several hours every day with their electrical impulse machines, I do not know of any externally applied electrical or mechanical method which can prevent significant heart atrophy. Only regular and sustained aerobic exercise can do that.

The case of Paula Radcliffe’s injured knee is relevant in this context. She had had this, quote, "little niggle" for a while before [recklessly] making it worse by defending her World Cross-Country title just a month before a potentially much bigger pay-day for her debut marathon in London. It was reported that physiotherapist Gerard Hartman had worked on the knee for three hours a day for ten consecutive days before she decided on the Thursday before London that she would run.

But brave-but-foolish Paula had been able to continue to run over 100 miles per week, thereby preventing the significant degree of heart muscle atrophy which a 10-day break from running would have caused. By contrast, young Beckham was on crutches with his foot in plaster for the first of his 7 week lay-off : there is no possibility that his heart size and hence aerobic fitness could have been restored by just two week’s worth of "light training" prior to the Sweden match.

After the match against Greece which had secured England’s qualification for these World Cup Finals, the Sports pages told us that Captain Marvel’s display had included not only scoring that dramatic equaliser in stoppage time, but also, quote, "running an incredible 16 kilometres in the course of the game". A sly piece of journalistic deception that : not only using km to describe a distance which the vast majority of readers would imagine to be much further than the 10 miles it is, but also omitting to mention that that 9-minute miles is no pace at all for a really fit 26-year old athlete.

Cometh the hour, cometh the not-fit-enough man. Beckham made one significant contribution by taking the corner which resulted in a goal conceded by a ball-watching defence. Shortly afterwards a pass into space down the right wing by Man United clubmate Paul Scholes was just that, a pass into space because Beckham had not even attempted to make the overlap. Manager Sven Goran Eriksson kept him on until after the Swedes had equalised, claiming that "David was tired, but I hope he will play for the full 90 minutes against Argentina".

Perhaps he will, but there’s no chance that he will be able to run 16km then, because for a weakened heart to grow again to its previous size and strength it takes at least as long as the lay-off which caused it to atrophy. The soccer pundits, none of whom I guess would ever have run 16km in 90 minutes, certainly nowhere near the 45-minute world record pace of a proper athlete, all said Beckham was "short of match fitness". As if the only way for a runner to regain aerobic fitness after an injury is to race. If that were so, there would be no point in training at all, be it 20 or 120 miles per week, would there?

Without a fit Beckham, its only world-class midfielder, England cannot reach the Final, but there is not enough time left now for Beckham to get fit before the Final. Oh!