A recent study examined the effects of a sixweek high-intensity interval training programme, followed by two weeks’ recovery, on iron status in trained cyclists.(1) Dietary intake was monitored to ensure that iron intake remained consistent throughout the study, but by the end of week three, haemoglobin, haematocrit and red blood cell count (three different markers of iron status) were all depressed. Meanwhile, serum ferritin (a blood protein involved with iron storage) decreased significantly by week five and remained depressed even in the recovery phase. Total iron binding capacity (TIBC – a measure of a blood protein that transports iron from the gut to the cells that use it) was significantly increased after three weeks, suggesting low iron stores. And the researchers suggested that this reduction could be sufficient over time to have an adverse effect on aerobic cycling performance.
Iron loss as a result of endurance exercise has been confirmed in other studies. For example, a large and comprehensive study examined the effects of different types of exercise on the iron status of 747 athletes divided into three groups (power, mixed and endurance sports) compared with untrained controls.(2) The researchers found that the endurance athletes had reduced levels of haemoglobin and haematocrit which was mainly attributable to exercise-induced plasma volume expansion: in other words, the same amount of iron carrying compounds were present, but diluted in a larger volume of plasma. However, they also found that physical activity of increasing volume and duration led to decreased ferritin (an iron storage protein) levels, which were particularly pronounced in runners. This was probably a result of haemolysis – the breakdown and destruction of red blood cells caused by the physical pounding action of running, leading to the release and loss of iron.
This effect of endurance training on iron status has been demonstrated even in very young athletes. An eight-month study examined elite swimmers in the 10-12 age bracket and compared them with non-active controls.(3) Although swimming is regarded as a ‘non-traumatic’ activity, during the competition phase the elite swimmers suffered significant decreases in serum ferritin and iron stores by comparison with the controls.
At the same time, the swimmers showed significantly higher levels of a new and highly sensitive indicator of tissue iron status known as ‘serum transferrin receptor concentration’ (STFR). When cells require more iron, they signal this need by increasing the number of transferrin receptors on their surface; a small proportion of these receptors actually come off the cell surface and are carried into the blood stream, where they can be measured. A high serum transferrin receptor concentration is, therefore, related to iron deficiency at a truly fundamental level – within the cells or tissues.
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However, although many previous human studies have found suggestive relationships between mild iron deficiency without anaemia and reduced aerobic performance, many of these findings have failed to reach statistical significance – ie the results were not sufficiently clear cut to draw reliable conclusions and were probably clouded by the inclusion of subjects with both normal and deficient tissue-iron status.
The problem has been that until recently there has been no definitive test for a real ‘tissue iron deficiency’. While measures like serum ferritin, total iron binding capacity (TIBC) and transferrin saturation do give a much clearer picture of an athlete’s iron status than a simple blood haemoglobin test, they still don’t tell the whole story – only whether an athlete is within certain ‘normal’ ranges.
They say that every cloud has a silver lining, and it seems that a really definitive test has emerged from the battle to detect erythropoietin (EPO) abuse in athletes. The use of EPO to artificially enhance the red blood cell count (and therefore the blood’s oxygen-carrying capacity) in endurance athletes is believed to have become widespread during the mid-to-late 80s; and in the search to come up with a reliable test for possible EPO abuse, a new marker of iron status was identified – serum transferrin receptor concentration (STFR). As we’ve already seen, STFR is an excellent indicator of tissue iron status because it actually shows how ‘hungry’ the cells are for iron.
A marker of iron status
The use of STFR as a marker of iron status is at the centre of some very new US research, which suggests that tissue iron deficiency without anaemia can not only impair aerobic performance but also blunt the adaptations that occur following aerobic training. In the first study, 41 untrained iron-depleted but non-anaemic women were randomly assigned to receive either a twicedaily iron supplement or placebo for six weeks.(11) From week three of the study, all the subjects trained on cycle ergometers five days a week.
As expected, iron supplementation significantly improved several markers of iron status, including serum ferritin, transferrin saturation and serum transferrin receptor (STFR) concentrations, yet this occurred without affecting blood haemoglobin concentrations or haematocrit. And, while the average VO2max and maximal respiratory exchange ratio (a measure of how efficiently oxygen is used in aerobic metabolism) improved in both groups after training, the iron group experienced significantly greater improvements in VO2max.
When the researchers analysed the results for relationships between the iron status markers and the measured improvements, it became apparent that it was the STFR concentrations that held the key. In the women whose STFR levels had been greater than 8mg per litre, taking extra iron produced a significant increase in VO2max above and beyond that produced by training alone; (remember, higher STFR levels indicate that the cells are signalling they need to take up more iron). Conversely, in women with STFR levels below 8mg per litre there were no significant benefits to iron supplementation.
The same researchers followed up with another study designed to investigate the role of tissue iron status in the impairment of endurance adaptation, using STFR as the main marker of tissue iron deficiency.(12) Using a very similar testing protocol, 51 iron-depleted but nonanaemic women were selected and randomly assigned to supplementation with either iron or placebo, undergoing five days a week of training on the cycle ergometer (between 75 and 85% of max heart rate) from week three of the six-week supplementation period. At the end of the study, all of the women completed three consecutive 5k time trials with only a short rest between trials. STFR measurements were taken at the beginning, middle and end of the study.
The researchers were particularly interested to see what differences emerged between women with raised levels of STFR and those without, and also how the former were affected by iron supplementation. The results showed that it was the raised STFR group who benefited from iron supplementation, working at a significantly lower percentage of their maximum work capacity during the first and second 5k bouts (indicating improved aerobic efficiency) and showing the largest overall improvement as a result of the training regime, especially by comparison with raised STFR subjects on placebo.
This placebo group reduced their time trial times by an average of only 36 seconds, compared with 3mins 24secs for the raised STFR/iron supplemented group. Moreover, the raised STFR/placebo group had to work at a higher percentage of their VO2max than the iron group for their relatively negligible improvement! Given that all the women in this study were assessed as iron depleted but non-anaemic, the researchers came to two main conclusions:
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[*]Iron depletion as measured by serum ferritin was not a reliable indicator of how the women adapted to training. All the women in the placebo group had depleted serum ferritin, but only those with raised STFR suffered an impaired training response. Moreover, in the iron group extra iron only helped those with raised STFR levels. While iron raised serum ferritin levels, it did not produce any significant performance increase in women whose STFR was already below the 8mg per litre baseline. It appears, therefore, that STFR is a far more reliable measure of a truly ‘functional’ tissue iron deficiency;
[*]iron tissue deficiency not only reduces VO2max but also impairs the body’s ability to adapt to an aerobic training load (probably due to a decrease in the iron-containing proteins involved in aerobic energy production), with serious implications for athletes!
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Testing for iron status is also far from straightforward. A low blood haemoglobin (Hb) measurement only appears in the very advanced stages of iron deficiency. It’s perfectly possible to have a normal blood Hb level while suffering severe effects from a tissue deficiency.
However, the latest research suggests that, although better then Hb alone, even these tests are insufficient to assess the real need for iron at the cellular level. For example, a reduced serum ferritin concentration generally indicates depletion of the iron stores; but, as the studies mentioned above showed, a reduced serum ferritin does not necessarily mean that performance will suffer because tissue iron stores may not actually be depleted. Serum ferritin is also what’s known as an ‘acute phase protein’, which means that concentrations are raised during inflammatory conditions. Thus, serum ferritin may be normal (or even raised) in an athlete with such a condition even if he or she is genuinely iron deficient. To determine the real need for iron, a serum transferrin receptor test is the best on offer, although it is relatively new and may not be readily available from your GP.
_http://www.pponline.co.uk/encyc/iron-deficiency.html
