Blood
Oxygen transport, clotting and the immune system in five litres. What a measured seven per cent increase in haemoglobin means in terms of performance, how often androgens raise the haematocrit, and why the equation ‘thick blood equals thrombosis’ doesn’t quite hold true.
Auch bekannt als: Blut, Hämatologie, Erythrozyten, Hämatokrit, Hämoglobin, EPO, Thrombozyten
What blood is made of
About five litres, just under eight per cent of body weight. If a sample is left in the centrifuge, it separates into two parts: the cells at the bottom, and the plasma at the top. The proportion occupied by the cells is the Hematocrit, and it consists almost entirely of red blood cells. Everything else is a thin layer in between.
- Red blood cells: sacks full of kernels Haemoglobin, 120-day service life, responsible for oxygen transport. They provide the mass and determine the flow properties.
- Leucocytes: the defence, see innate and adaptive immune defences. In terms of numbers, it is a minor factor, but not in terms of function.
- Platelets: Cell fragments that form the initial wound seal , see Blood clotting.
- Plasma: Water containing albumin, clotting factors, electrolytes and nutrients. Its volume fluctuates with the fluid level and thereby shifts the proportion of each cell type measured, without a single cell having changed.
Motif: Two narrow, vertical glass tubes side by side, both filled to the same level. In the left-hand one, the dark column of cells at the bottom occupies slightly less than half the height of the tube, with clear, yellowish plasma above it. In the right-hand one, the column of cells extends significantly higher, to just under six-tenths of the height, whilst the plasma above it is correspondingly narrow. Between the cell column and the plasma in each tube is a wafer-thin, pale line forming a layer of leukocytes. On the side is a scale in tenths connecting both tubes . Purpose: explains haematocrit in terms of what it actually is – namely, a volume fraction – and illustrates why a high value makes the blood more viscous. Style: flat, factual vector graphic in the style of a textbook blackboard, clear contours, few flat colors, no photorealism, no textures, no drop shadows, no spatial lighting, calm monochrome background, no text in the image. Label: Plasma, leukocyte layer, erythrocytes, 45 per cent, 58 per cent. Format: horizontally, roughly 16:9, with the tubes centred and plenty of space on either side.
How oxygen transport works
Haemoglobin
A red blood cell contains around 270 million haemoglobin molecules, each of which binds four oxygen molecules to a single iron atom. The bond is deliberately imperfect: it becomes weaker when the environment becomes more acidic, warmer, or when there is a high concentration of carbon dioxide. This is precisely what happens in working muscles, which is why the blood releases more oxygen there than elsewhere. The connection with the Acid-base balance and with Lactate is therefore not a side effect, but the regulatory mechanism itself.
Why ‘more’ is not necessarily better
More red blood cells mean greater transport capacity, but also thicker blood. The viscosity increases disproportionately with the cell content, and beyond a certain point, the additional resistance requires more cardiac effort than the extra oxygen provides. Where this point lies depends on the individual. The statement ‘higher haematocrit equals greater endurance’ therefore only applies over a limited distance; see Cardiovascular system.
The scheme
Oxygen sensor in the kidney regulate the release of erythropoietin, which in the bone marrow Haematopoiesis drives. This control loop is the objective of Altitude training, from injected EPO and, indirectly, from androgens.
What the studies show
How much of a difference does having more haemoglobin really make?
48 trained adults, half of whom were women, were given, in a double-blind trial over four weeks, either low-dose epoetin beta or saline solution. The total haemoglobin mass increased by 6.7 per cent, performance in the time trial by 4.1 per cent, and maximum oxygen uptake by 4.2 per cent. In the placebo group, there was no change.
The figures are clear, yet they require closer scrutiny than they appear to suggest. For the three performance metrics, the variation is greater than the effect itself: individual participants did not become faster. The only thing that is certain is the increase in haemoglobin, and that is what was measured, not what matters. Furthermore, there is no evidence whatsoever to support this in relation to strength training. Oxygen transport does not limit a heavy set of squats; it only does so when Endurance activities for minutes.
How often does the haematocrit rise when taking testosterone?
A systematic review of 45 studies on drug-induced erythrocytosis found rates of up to 66.7 per cent during testosterone therapy, in both men and trans men. Thromboembolic events occurred in up to 2.7 per cent of those treated. A clinical guideline identifies erythrocytosis as the most common side effect of testosterone therapy overall and recommends reducing the dose or discontinuing treatment if the haematocrit level exceeds 54 per cent, until the level returns to normal.
This applies to medically supervised substitution; see Testosterone. When it comes to dosages in sport and highly androgenic substances such as Trenbolone According to user reports, the increase is regularly higher than this, but there is no verified data on this.
When does it become dangerous?
This is where things become more complicated than the widely accepted rule of thumb suggests. A review article examining whether haematocrit itself determines the risk of thrombosis reaches a different conclusion: in most forms of erythrocytosis, there is actually no increased incidence of thrombosis, and in certain circumstances, the risk actually rises following bloodletting. The authors attribute this to the fact that cellular properties, rather than the volume fraction, are the deciding factor.
Two findings that do not contradict each other, but are often played off against one another. It has been observed that, under the influence of testosterone, both erythrocytosis and thromboembolism are more common. It does not follow from this that the haematocrit level is the causative factor, and the overview of erythrocytosis suggests otherwise. In practical terms, this means that the 54 per cent threshold is a useful benchmark for taking action, but there is no threshold level, and a value just below it does not mean it is safe. The idea that the blood becomes ‘too thick’ and therefore clogs the blood vessels is the most vivid, yet at the same time the least well-supported, explanation.
What puts a strain on the blood
Erythrocytosis caused by androgens
What happens: Androgens stimulate erythropoiesis via several mechanisms simultaneously. One of the mechanisms thought to be involved is reduced hepcidin production, which makes more iron available for blood formation. The pathway has been described; the outcome has been measured: haemoglobin and haematocrit levels rise, as shown in the systematic review in up to two-thirds of those treated.
What it depends on: depending on the dose, route of administration and substance. The review found the highest rates among those undergoing testosterone therapy. The fact that short-acting injections with high peak levels drive the value up more than steady-state profiles is the commonly accepted clinical explanation; however, this cannot be substantiated by the studies reviewed here. What follows from this is: The value fluctuates over weeks or months, not days. A single measurement without a trend tells us little, and is only useful if the fluid level is normal.
What you can do: Firstly, the cause: reduce the dose and switch to more consistent levels. The clinical guidance sets the threshold for action at 54 per cent. Bloodletting or blood donation reliably lower the level, but are not without consequences: they deplete iron, and when carried out repeatedly, they cause iron deficiency, the effects of which on the flow properties of cells are explicitly discussed as a possible risk factor in the overview on erythrocytosis. Bloodletting is therefore a stopgap measure rather than a long-term solution.
Iron deficiency
What happens: Without iron, there is no haemoglobin. In athletes, three factors come into play: increased demand, increased loss and reduced absorption, because the physical exertion itself causes a short-term rise in hepcidin levels. Performance is already affected even before the actual anaemia sets in.
What it depends on: Gender, intake and extent of exercise. The review cites a ferritin level of 30 micrograms per litre as the threshold for athletes over the age of 15, and 50 prior to a stay at altitude. What follows from this is: Ferritin should always be included in blood count tests, otherwise an iron deficiency may be overlooked as a ‘normal blood count’. It should be noted that ferritin levels rise in the presence of inflammation, thereby masking a deficiency.
What you can do: Intake via diet, otherwise Iron as a supplement. Two check-ups a year are sufficient. Continuing to take supplements when ferritin levels are normal serves no purpose and is expressly not recommended.
Drainage as a false finding
What happens: If plasma volume falls, the measured cell proportion rises, even though not a single cell has been added. A haematocrit of 55 per cent following pre-competition dehydration is different from the same value in a balanced state, even though the laboratory reports both as the same figure. Conversely, the increase in volume resulting from endurance training lowers the value without any cells being lost.
What it depends on: on the fluid levels at the time of the test, and on how long beforehand the athlete had been training. What follows from this is: A single high reading does not justify a bloodletting. What you can do: Always measure under comparable conditions: in the morning, on an empty stomach, without having done a strenuous workout the day before and without running Drainage, see Hydration and Peak week.
Monitoring
- Haematocrit and haemoglobin: as a trend under the same conditions. 54 per cent is the threshold at which trading takes place.
- Ferritin: is part of this, even when haemoglobin levels are normal. Threshold: 30 micrograms per litre.
- Red blood cell indices: MCV and MCH indicate whether an iron deficiency is the underlying cause or whether there is another problem.
- Platelets and white blood cells: are part of the complete blood count, but their levels do not fluctuate regularly in the presence of androgens.
- Please bear in mind the context: The haematocrit is one of several values that are interpreted in conjunction with one another; see Laboratory monitoring and Cardiovascular risks associated with AAS.
Classification
For strength athletes training without supplements, the blood test is primarily a matter of iron levels, and that’s where it’s worth it: a deficiency reduces performance before it becomes apparent as anaemia, and it’s inexpensive to remedy. Haematocrit is not an issue in this group.
Anyone using androgens is likely to experience erythrocytosis, the most common side effect of all, with rates of up to two-thirds. The correct response lies in the dose, not the needle, because repeated bloodletting deprives the body of iron and may therefore merely postpone the problem rather than solve it .
As far as endurance is concerned, the gain is measurable and limited: just under seven per cent more haemoglobin mass resulted in around four per cent greater performance in the time trial, with a margin of variation that includes some participants who saw no improvement at all. The biochemical principles and detection methods for blood doping have long been described.
The question that carries the greatest practical weight remains unanswered: at what level, in the case of an androgen-induced increase in haematocrit, does the risk actually arise? According to this review, it is not the volume percentage alone. Until this has been clarified, the 54 per cent mark remains a convention with practical utility rather than a biological limit.
Sources
- Gordeuk VR, Key NS, Prchal JT. Re-evaluation of hematocrit as a determinant of thrombotic risk in erythrocytosis. Haematologica. 2019. PubMed
- Lippi G et al. Biochemistry, physiology, and complications of blood doping: facts and speculation. Crit Rev Clin Lab Sci. 2006. PubMed
- Liu J et al. Diagnosis, management, and outcomes of drug-induced erythrocytosis: a systematic review. Blood Adv. 2025. PubMed
- Agrawal P, Singh SM, Kohn T. Management of erythrocytosis in men receiving testosterone therapy: clinical consultation guide. Eur Urol Focus. 2023. PubMed
- Breenfeldt Andersen A et al. Microdoses of recombinant human erythropoietin enhance time trial performance in trained males and females. Med Sci Sports Exerc. 2023. PubMed
- Clénin G et al. Iron deficiency in sports: definition, influence on performance and therapy. Swiss Med Wkly. 2015. PubMed
This article was created using AI systems. Find out more