The data which form the basis of this article were collected during two series of experimental trials at the Sport and Exercise Science Research Centre of South Bank University, where I am a postgraduate research scholar. While we were not investigating haematocrit itself, we customarily measure it because doing so enables us to determine the extent to which plasma volume is altered by exercise, and thus to correct the results of assays which measure the concentration of substances in the blood.

During the course of our experimental work we collected quite a large body of haematocrit (Hct) data - 66 measurements from 22 male subjects, aged from 22 to 40 years and with a spectrum of fitness from the completely sedentary to elite athletes, both endurance trained (cyclists) and strength trained (power lifters). These data present us with an opportunity to shed some light on questions such as:

• What is the range of 'normal' Hct ?

• How, if at all, does Hct change with training ?

• Is there any correlation between Hct and endurance athletic performance ?

All measurements were made in the afternoon or early evening; subjects were asked to ensure that they came to the lab well hydrated. If, for each subject, we take the mean of all his measurements as being the most representative individual Hct, we have 22 measurements. These follow a statistically normal distribution – that is, they are distributed in such a way that the majority of the 22 values are grouped around the mean, with progressively fewer values occurring as we depart further from the mean, either above or below it. In this representative sample of the British male adult population, the mean Hct was 42.2% and the standard deviation (SD) 2.5 percentage points. That is, on the basis of this sample 68% of the whole population of British males aged 22-40 might be expected to have values within 2.5 percentage points of 42.2%, and 95.5% might be expected to have values within 5.0 percentage points of 42.2%.

The highest value recorded was 48.0%, and this was something of an outlier, the next highest being 45.5%. Serum osmolality (a measurement of the concentration of dissolved molecules in the blood) indicated that this high result was genuine, and not attributable to dehydration; so there do appear to be a few people with unusually high haematocrit which is nevertheless normal for them. The subject in question, at 2.3 SDs above the mean, was one of 1% of the population to have a Hct that high.

So the question arises: 'To have the potential to become an elite endurance athlete, do you need to be in that "lucky" 1% ?' Since we also have for each subject the results of at least two maximal oxygen uptake tests, an answer is available from our data. A Spearman correlation test indicates that there was no correlation between VO2max and Hct (p = .427). In other words, it was unnecessary to have a high Hct to achieve a good result in the VO2max test. It therefore appears that it is not necessary to be blessed with a naturally high Hct to become a good endurance athlete. In fact, our subject with 48% Hct, while a trained club runner, was a fairly modest performer in the cycling VO2max test, at 49 ml/min/kg.

We can also examine the data in another way: does endurance training alter an individual's Hct? Looking at two subsets of the subjects will give insight into this question. We have a group of 6 very sedentary individuals, whose mean voluntary physical activity in the year preceding testing was 1.4 hours/week (and this includes activities such as gardening), and whose mean VO2max was 36 ml/min/kg. We also have a group of six well-trained (but not elite) cyclists, whose mean VO2max was 61 ml/min/kg (these are the sort of riders who are capable of winning 3rd-cat road races and local open time trials). None of the cyclists was altitude trained, and I consider them most unlikely to have had access to, or the desire to use, blood doping or boosting techniques. If training alters Hct, we might expect the cyclist group to have different values to the sedentaries. In fact, there was no difference between Hct in the two groups (p = .335). So chronic endurance training has not given the cyclist group a different Hct to the sedentary group. Their greater oxygen transport capacity is attributable primarily to a larger cardiac output – in other words, their hearts can pump more blood per unit time.

We also have repeat data for the same sedentary subjects after twelve weeks of supervised exercise training (running, cycling and rowing) designed to improve their aerobic fitness. There's no doubt that the training worked: VO2max increased by at least 10% in every subject, to a new mean of 43 ml/min/kg. But did Hct change? Statistically, no (p = .074). It did show a trend towards a statistically significant change, but not in the direction you might expect – Hct after training (mean 40.1%) tended to be slightly lower than before training (40.9%). This is probably explained by the well-known phenomenon of 'athlete's anaemia' – exercise training may increase plasma volume more than red blood cell count, making Hct (the percentage of the blood which comprises cells) slightly lower. In any case, twelve weeks of aerobic training did not increase Hct in our subjects. Their VO2max gains came principally from the same adaptation seen to a greater extent in the cyclists' increased cardiac output.

So we would not expect very highly trained athletes such as elite cyclists to have increased their Hct by the large volume of training they do; nor does it look as though to reach the top in cycling it is necessary to have been blessed with a naturally high haematocrit. I would expect the Hct of a representative professional cyclist to be not very different from the 42.2% mean of our subjects. Conversely, I would assume that any athlete whose Hct exceeded 48%, and who had no record of previous similar high measurements, had boosted his red blood cell count by means legitimate (altitude training) or otherwise (blood doping, EPO).

What about more acute effects of exercise on haematocrit? Blood pressure is increased by exercise, and this tends to drive plasma out of the circulation through gaps between the cells which make up the walls of blood vessels. Additionally in long events such as Tour stages, especially in hot weather, it is impossible to replenish fluid at the same rate as it is lost in sweat, so that plasma volume is further compromised by dehydration. All the cells, though, remain in the circulation, with the result that the blood becomes increasingly turbid. The heart is forced to meet an exercise-imposed high demand for cardiac output while pumping more-than-normally viscous blood.

After their first VO2max test, all but two of our subjects did a second progressive test, in which the rate of incrementation of the work load was calculated to give a predicted test duration of 25 minutes, regardless of fitness. Blood was sampled before exercise and immediately following exhaustion. If we look at the acute change in Hct between the beginning and end of this 25-minute test, we get some idea of the extent to which Hct might change during a short cycling event.

At the point of exhaustion, mean Hct had increased by an average of 5.8 percentage points. The highest Hct was seen in two subjects, in whom it rose to 52.5%. As well as being of short duration (and low to moderate intensity until the last 5 minutes or so), the exercise test was conducted in an air-conditioned room in which the temperature was maintained at 21°C. Dehydration was probably not a major factor. I assume that Hct would increase considerably more by the end of a long tour stage ridden on a day of 38°C temperatures. I can only guess at the stress placed on the heart by pumping blood which had started that stage at 49.9% Hct.

What about the rider who, when found to have a Hct above 50%, claims that he doesn't understand why his result should have been so high on that day, and that his usual result is well below 50% – is there considerable naturally-occurring variation in an individual's haematocrit ? Our data indicate that there is some intra-individual variability of Hct, but do not include sufficiently extensive repeat testing to allow valid statements to be made about the extent of this variability. In the context of cycling, however, it can be said that:

• blood sample collection must be carried out with a sufficient interval after racing or training to allow for full rehydration – a team doctor who is doing his job will in any case ensure that riders are rehydrated prior to their next day's racing or training

• a standard posture must be adopted for sampling, and the rider should rest quietly in this position for ten minutes prior to sampling.

These measures will minimise the variability of any individual rider's Hct result, and competent testers understand the need to apply them. Nevertheless, scientific work is urgently needed to determine the extent of day-to-day variability of Hct in elite endurance athletes. Having such data would allow us to formulate sensible rules for the allocation to each individual athlete of a 'personal norm' for Hct based on a history of repeated testing. Any marked deviation above this norm could then be used to justify suspension from competition. This would be safer than setting an arbitrary level of 50% Hct for suspension – a limit which appears in any case to be higher than is likely to be achieved without some form of intervention, legal or not.

There are three strategies for increasing haematocrit: altitude training, blood infusion and rhEPO use. Altitude training has drawbacks, both practical and physiological (although these may be overcome to some extent by the use of a hypobaric chamber to simulate high altitude). Blood infusion of donor blood is detectable, because of small differences between blood from different individuals of the same blood group. Autologous blood doping, that is the reinfusion of one's own blood, has the disadvantage that after extraction of the necessary 2 to 3 pints of blood, recovery of normal haematocrit takes 4 to 8 weeks, during which time training is compromised.

rhEPO (recombinant human erythropoietin) is easily given by subcutaneous injection, and stimulates bone marrow cells to increase red blood cell formation – it has a legitimate therapeutic use in anaemia. In exactly what circumstances rhEPO enables an elite athlete to increase performance is a more complex question than it might at first appear, and rather beyond the scope of this article. The timescale of the response to the drug requires that it be administered weeks or months prior to the target competition. Abuse is difficult to detect, because the pharmaceutical product is a manufactured analogue of a naturally occurring hormone; however, there are subtle differences between natural and manufactured erythropoietin, and progress is now being made towards a method for detecting these differences in blood samples.

In the meantime, I would suggest that as soon as possible any cyclist applying for elite status or taking up a professional contract should have to supply evidence of a personal Hct norm by producing not less than 10 Hct measurements from a preceding period of not more than 2 years. It should become the responsibility of recognised 'nursery' clubs, or in Britain the responsibility of the World Class Performance Program, to ensure that any aspiring elite/professional rider is regularly checked. Testing would be maintained during an elite/professional career, so that every rider would always have the necessary data to offer to a new team. Routine tests would continue during the closed season and irrespective of injury.

Of course, there are ethical, legal and financial questions bound up in this issue, too. Blood testing is an essentially intrusive procedure in a way in which urine testing is not, and a programme of routine testing would require a significant investment in staff to collect samples, laboratory facilities to analyse them, and secure data storage systems for the test results. But only blood tests will detect the methods used by up-to-date cheats.

Our sport and others have been greatly undermined by repeated doping scandals over the past several seasons, to the extent where an athlete cannot win a major race without his or her performance being assumed by some to be attributable to dope. If the sport we love is to avoid being reduced to a mere spectacle, it is imperative that national and supranational governing bodies grasp the nettle of imposing effective measures against cheating with no further delay. This means that they must recognise that for each elite athlete, regular blood testing to establish a personal history of Hct results (and of other factors such as testosterone and growth hormone status) should be a precondition for competing at the highest level. It will also be necessary for elite athletes to accept that a history of regular blood testing is a necessary qualification for their chosen profession. After all, it's in their interests too.