I have three new research projects on the go now, continuing the Experiment of One which the late, great Dr George Sheehan advised all readers over 35 of the US edition of Runner’s World to embark on ("because you’re the only one who is interested in finding out what works for you").

PERFORMANCE ENHANCING ORTHOTICS. First, I eventually got through the NHS waiting list to meeting a specialist in the, er, Musculo-Skeletal Unit at St James’ Hospital to ask if he could get my knees back to how they were when I was able to walk upstairs without pain. And, as an added bonus, ditto when out running. The x-rays had shown a thinning of the cartilages behind the kneecaps – not unusual in wrinklies, he said, so nothing can be done about that – which means that not enough of the heel-strike force is being absorbed before it gets to the adjacent bone. Which is why it hurts, he said.

He then told me that I am striking the ground on the wrong edge of my heels, i.e. I’m a supinator, not a pronator like 85% of runners are, and that the condition could be relieved by orthotics. So I was fitted with a pair of soft ones having a "Puron" wedge stuck on the underside of the insole and angled at 2° from the inside edge to the outside edge of my heel. Remembering George’s unhappy experiences with hard plastic ones, I was astonished when the pain of the stairs and of running had gone within a week of my first wearing them. So I’ve booked to run in the Portland Marathon on September 30^th while I’m over in Oregon "visiting with" – as Americans say – my elder daughter and her growing up family, both the two boys of which, aged 13 and 15, are now taller than I am as they have been growing while I’ve been shrinking (because of thinning discs, I’m told).

My first run with the orthotics in was on June 22^nd, which meant I had just 14 weeks to prepare for the marathon. I was starting from a base of a resting heart rate of 57bpm and just 189 miles, 15 miles a week, covered in the previous 3 months reference period. With 10 of those weeks now gone, my pace over my twice 2-mile loop is around 30 seconds a mile quicker, although for various priorities and reasons which seemed right at the time I’m only getting in 22 miles a week even now. My resting heart rate is down to 44, which means that the amount of blood/oxygen pumped round my pipes when I’m at rest has increased by a whopping 30%. So far, so good.

BIGGER, BETTER HEART. Which brings me to the second experiment. All our energy for running is derived from the chemical combination of oxygen with carbohydrate and fat in our muscles, so the more oxygen we can pump round the system per minute, the more energy will be generated and the further we shall go each minute. The question is what do I have to do to increase that oxygen supply : the answer is to get my heart to grow (instead of shrinking because I have not been taxing it enough while my poorly knees have been so painful). We get bigger muscles by putting more strain on the ones we’ve got than they can easily cope with, whether by running faster, further or by more muscle-specific weight training in a gym, and we can get a bigger heart by demanding more oxygen supply from it than it can supply readily.

It so happened that I had an appointment to see haematologist Dr Mano Rajah at the beginning of August for my biannual check-up. Everything was normal apart from three enzymes which were way over the top, the very same condition which led to my first appointment with him 17 years ago. It is caused by "hypoxia", which is medicalese for a shortage of oxygen supply to, in this case, my liver. It is usually the result of anaemia.

But I’m not anaemic now, as I was in 1984 when I was running 55 miles a week at 7:15 pace and racing a 3:00 marathon in London. No, what I am doing, deliberately now because I have a heart rate monitor to guide me, is to run my 4-milers so that I sustain a working rate of over 150bpm for at least 5 minutes out of the 32 to 34 minutes of the session. Because I’m sure my shrunken heart could not sustain that for even one more lap, I must be well over my current lactic threshold by the time I finish.

We die if too much lactic acid builds up in our blood for too long, so the liver has to work like crazy to oxidize it back to carbohydrate, for which it needs huge supplies of the aforesaid enzymes. Simple, really, just a shame that it’s taken me 17 years to realize that’s how I grew that bigger heart in 1984 when my resting pulse rate was down to, er, 34bpm in the week I first saw Dr Rajah.

It was funny, really, because the symptoms I had are more usually associated with heavy drinking and that was indeed the reason in the case of another of his patients at the time, a senior dignitary of Leeds. This other guy was an alcoholic and, inter alia, he had a resting pulse rate of 80bpm. I shall always remember the look of incredulity on Mano Rajah’s face as he stared at my electrocardiogram that first day. "We get concerned about anyone with a heart rate of less than 45", he said, "because it is a warning sign that the heart may suddenly stop altogether".

Yes, I realise that the 155bpm I reached on my run the day before the blood test and the 162bpm on two other occasions are well over 100% of the maximum heart rate possible for a normal 74-year-old. But anyone who runs 4 miles a day, aged 24, 74 or whatever, flat out or jogging, cannot be categorized as "normal", so I don’t pay any attention to what the chart in the doctor’s waiting room says ’cos I’m sure the guy who drew it has never heard of crazy blokes like me.

That’s no excuse, incidentally, for the Polar HRM booklet to print the same "maximum heart rate is 220 minus your age" chart and for the Polar staff on their Stand at the London Marathon to try to justify such nonsense when I tell them it’s stupid. They would have me doing most of my "training" at a maximum of 70% of 146, i.e. 102bpm, which I can reach at a fast walking pace. It isn’t at all clear to me what training effect Polar believes that might have. They’ve never considered it, I suspect. Conversely, the last time I was fit for racing, I ran the second half of the 5000m at the WAVA Games at an average heart rate of 168, so I guess that was my lactic threshold at the time. If that were, say, 90% of my actual maximum heart rate to exhaustion, it would calculate to being 187bpm and 85% of that, the maximum recommended by Polar, to 158. Which fits in far better with how I actually train than easing off when I reach 102 !

So I shall keep blasting round my circuit for the next couple of weeks before I go to America, maintaining my "excessive" heart rate for long enough to get down to a resting pulse rate of somewhere between 38 and 42 and hence to sub-8 minute miles.

HY, DE-HY. The third experiment is about hydration and dehydration. I have been particularly interested in it since erythropoietin, EPO for journalistic short, appeared on the drugs-in-Sport scene. I had asked Dr R if it would better for curing my chronic anaemia than the ferrous sulphate/folic acid/vitamin B₁₂ he had been prescribing me for the previous 13 years. He said a) it’s for kids who would otherwise die because their Hgb counts are like 6 to 8, b) it costs over £150 a shot and c) the outcome is uncontrollable and d) it wouldn’t be ethical for me to prescribe it for you because I have no reason to believe that your kidneys are making less of it than you need. I was glad he said that because the tablets are much less expensive and more effective than going down to the Pyrenees for a month’s worth of "altitude training" twice a year – as Protesta Paula does to boost her red cell count – and I don’t have the time for that anyhow.

It’s one thing to have blood which complies with the normal standard of the average couch potato, even if it is towards the anaemic end of the range. It’s quite another to be towards the opposite end and having 30% or so more red cells floating round one’s system. I have gone on at some length before about what I have described as the "Ketchup and Red Wine Effect", i.e. have too many red cells and the blood is pumped so slowly that less oxygen is delivered to the working muscles than when it is anaemic.

The problem which endurance runners and Stage-race cyclists encounter because of dehydration is very similar to that which the middle distance runners hit because of lactic acid. There’s an elbow in the respective graphs, above which acid levels in their case and blood thickness in ours rise at a very steep angle, theirs due to hypoxia, ours to dehydration. The result is the same, it’s a rapid fall in racing speed.

They hit their Wall because they start too fast : in the 1997 IAAF World Championship 400m final, at 200m Iwan Thomas in lane 3 was level with, i.e. over 3 metres up on Michael Johnson in lane 4, but at the finish he was sixth, 15 metres behind. Thomas ran his second 200m 11% slower than the first 200 : that’s like 65 minutes for the first half of a marathon and 72 minutes for the second half and losing 20 places ! We hit our Wall because, if we dehydrate to the point that our blood is so thick that our oxygen delivery reduces, we use up our carbohydrate reserves SEVENTEEN TIMES FASTER than when there is enough oxygen to maintain our speed.

Not having raced properly since the Spring Handicap in April – and that the first time in over a year – and with no training runs longer than 4 miles either, I was very uncertain how I would fare over the 10k of the Summer Handicap. I did know, though, from that recent blood analysis that my haemoglobin count was over 15, my red cell count over 5 and my haematocrit percentage over 45, edging up towards the elbow of the curve where blood thickens rapidly. I also know that, as I start to sweat on the second lap of my training runs, my heart rate is always 3 to 5 beats per minute higher than on the first.

A little Experiment of One was called for. Allowing time for it to get through my stomach, 40 minutes before the race began I drank 400g/15oz/¾ pint of water. Before end of the first mile felt couldn't keep up 150 heart rate much longer; did; the whole of the return journey from halfway covered with a heart rate of between 149 and 151; averaged 148bpm overall; did it in 49:58, excluding 2 seconds each way getting through the kissing gate; that's worth between 3:46 and 3:49 in Portland. Which, if it works out like that, will be a couple of minutes faster than my slowest ever marathon – excluding the last two, part-walking Londons, of course – since my first in 1981 (which, incidentally, was the only time in 85 marathons I trained in the proper, orthodox manner with two long runs of over 20 miles and over 3 hours).

I was so pleased with that 10k run and the outcome of the experiment that I decided to continue it before my training outings. I was astonished by the results. Yes, the second lap was a) covered at almost the same heart rate as the first, which it never has been before, b) in the same time as the first or slightly quicker, which is unusual, but c) the overall time was a minute slower than it had been in the previous week without the drink and d) my average heart rate and the maximum reached were all of 10 bpm less !

I believe the explanation to be this. Provided my blood thickness is not too close to the haematocrit elbow, my heart will deliver the same volume of blood per beat, give or take, after its dilution by my drinking 400g of water as it did before it. So after the dilution, the amount of oxygen delivered per beat will go down, resulting in my running more slowly unless I increase my heart rate while out training by running faster. But I’m reluctant to do that because, not knowing where I am on the haematocrit/blood viscosity graph, I don’t want to hit the Wall at 3 miles. In the Handicap, however, I set out to maintain the same heart rate as when I’m training and I did : 148bpm average and a maximum of 156 going up the hill to half way.

WHAT NEXT? It still leaves me with the problem of how much extra to drink, if any, before the race in Portland. I’m going to be a lot more dehydrated running 26 miles on a hot day then than I was on a cool evening round the Res. There’s some more experimental work to do and no better time than in a race when there is nothing at stake except a little pride in not creating a disaster out of a fun day out with the grandchildren. So I’ll do what will provide me with the most useful information for when I’m racing in something important, write it all down before and up afterwards, and then assess the results before trying out something else next time.

It may be that I shall come up with an explanation why, in all those years when I was near the anaemic end of the NHS haematocrit range, my marathon times were always significantly faster than my equivalent 10k times. In the WAVA Age-Graded Tables, my 2:57 marathon PB is equivalent to a 38:23 10k, but my actual 10k PB is an Abbey Dash 40:10 – 39:70 in my own records, of course ! – which is a 4½ % slower than it should be.

And maybe that’s why world-class 10k runners seldom run world-class marathons first time out because, perhaps, they have too many red cells and the inevitable extra dehydration in a marathon pushes them past the haematocrit elbow. After several months of 120+ mile weeks, though, they will have done so much damage to their soft tissues and leaked away so many red cells that they will have drifted down towards having the well-known "runners’ anaemia", which is usually attributed to an increase in blood volume in the system, but perhaps the real underlying cause is the reduction of red cell volume.

Next time out the net dehydration they incur in the first half of the race will actually increase their rate of oxygen delivery in the second half. Then they go training "at altitude" to restore their red cell counts to "normal" and never run as fast a marathon ever again !