It is one of life’s paradoxes that the simplest things—on closer inspection—are often the most complex. And so it is with nutrition. Iron, for example, is one of the most familiar yet misunderstood nutrients. Most athletes know that iron is a mineral required for the formation of the red blood cells used to transport oxygen to hardworking muscles, and that an insufficiency of iron causes anemia.

Most athletes are far less aware, however, of the fact that iron is one of the most difficult minerals to absorb, and that they are especially vulnerable to iron depletion through training-induced losses—especially if their event involves endurance training. To make matters worse, its possible to have a healthy blood (Hb) count while simultaneously suffering from depleted levels of tissue iron. And, if that weren’t enough, new research has demonstrated that this tissue-level depletion impairs the body’s ability to adapt to endurance training.

To better appreciate the complexities of iron nutrition, it helps to understand a little about how iron functions in the body. Most of us are aware of its role in transporting oxygen molecules around the bloodstream to the working muscles; the red color of oxy-hemoglobin in our red blood cells is visible evidence of iron in action. When buried deep in the hmoglobin molecule, an iron atom has the perfect atomic structure to bind strongly enough with an oxygen molecule to be transported around the bloodstream (in the form of oxyhemoglobin) but, crucially, loosely enough to give up the bound oxygen to a muscle needing it.

If your iron status becomes severely depleted (through inadequate intake, poor absorption or iron losses), your blood hemoglobin levels will drop, leading to a reduction in your oxygen carrying capacity. The result is fatigue, tiredness and breathlessness, even after gentle exertion—the classic signs of anemia. Most doctors test for blood hemoglobin levels when they test for iron anemia, although there are other more relevant tests.

Iron is also crucial for a number of energy-releasing processes because it activates enzymes called catalyses, among others. In this role, iron functions as a sort of electron shuttle, passing electrons to and accepting electrons from other molecules thereby helping to make and break chemical bonds in biochemical reactions that would otherwise not occur.

Although as a plain metal iron is very stable and inert, it isn’t any good for humans. Biological systems need iron in its ionic form. Strip away two negatively charged electrons from an iron atom and you generate an iron ion, carrying two positive charges (abbreviated as Fe2+); remove a third electron and you get iron ion carrying three positive charges (Fe3+). The energy levels of the Fe2+ and Fe3+ ions are quite close, which means that these two ions can easily inter-convert by donating and accepting (i.e. shuttling) electrons. If a Fe3+ ion accepts an electron from a molecule in a biochemical reaction, it gains a negative charge and becomes Fe2+. If this Fe2+ ion then passes that electron on to a different molecule, it returns to its original Fe3+ state.

The positive charges carried by these iron ions means that they are easily attracted to negatively charged molecules, or parts of molecules, to which they can often ‘lock on’ and bind. This is particularly the case with the very strongly positively charged Fe3+ ions, which are attracted to and bind especially strongly with molecules containing negatively charged oxygen atoms. A good example of this strong binding is with carbohydrates, which are built from molecules with lots of oxygen-containing fragments. While many carbohydrate foods contain iron, the iron ions are sometimes bound so strongly that the process of digestion is not able to pluck them away. The iron stays joined to these carbohydrates as they pass through the digestive tract, and passes out largely unabsorbed.

If the iron is in the more positively charged Fe3+ state, this binding is even stronger than with the Fe2+ state because there is more attraction between the negative oxygens and the more positively charged Fe3+. This accounts for the poor iron bioavailability of many iron-rich foods: the iron is there but can’t be easily prized away for absorption. Even in foods whose iron is readily available, uptake can be considerably reduced by the simultaneous consumption of other food or drinks containing iron blockers such as tea, which contains tannic acid.

Another barrier to iron absorption arises from the fact that the cell walls of the digestive tract are electrically neutral while iron ions are strongly positively charged, making it hard to transport them across the gut wall into your body. However, iron that is chemically bonded to protein molecules (such as the haeme iron found in meat) carries no overall charge and is much more easily absorbed.

For all these reasons, iron nutrition presents a challenge. It is not just a case of consuming enough iron but of consuming it in a way that makes it fully available to your body.

Then there is the problem of iron loss, which is potentially greater than for many other trace minerals. In menstruating women, for example, monthly losses amount to an average 28mg, which can be easily doubled if periods are heavy or if intrauterine contraceptive devices are used. More importantly for athletes, there is a growing body of evidence that heavy training, particularly of the endurance variety, is a major cause of iron loss.

A recent study examined the effects of a six week high-intensity interval training program, 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, hemoglobin, 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. 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 hemoglobin 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 hemolysis—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.

Given that iron availability in foods is frequently poor, that iron is difficult to absorb and that training (especially endurance training) can deplete iron stores, it is hardly surprising that iron status in athletes has come under scrutiny. In the past, the age-old hemoglobin test was thought to be sufficient to determine an athlete’s iron status, the ‘normal’ range being 12-16 g/dl (grams per deciliter), with anything under 12g/dl signifying iron anemia. However, more recent research has indicated that you can be quite iron deficient without being diagnosed as anemic. This is because reduced blood hemoglobin is one of the very final stages in iron deficiency, and a lot of iron-dependent systems can suffer before this final stage is detectable.

A Canadian study found that although 39% of women had depleted iron when assessed by the more sensitive serum ferritin test, less than one tenth of these were identified as anemic by the conventional hemoglobin test!(4) Moreover, research increasingly shows that a low iron status without a corresponding low blood hemoglobin level impairs physical performance.

Another study found that women athletes who were not conventionally anemic but had a mild iron depletion as demonstrated by the serum ferritin test had significantly lower VO2max values than those with no iron depletion.(5) The researchers concluded that this reduction in VO2max was due to lower stored iron rather than reduced blood hemoglobin. They also demonstrated that when these women were given iron supplements, their serum ferritin values and performances improved without any apparent changes in blood hemoglobin.

Yet another study examined 40 young elite athletes with normal hemoglobin levels but below average serum ferritin.(6) The athletes were spilt into two groups and randomly assigned to a 12- week treatment with either iron supplements or placebo. Before and after the treatment, aerobic and anaerobic capacity was measured in both groups by means of treadmill tests. At the end of the study period, the iron-supplemented athletes recorded significant increases in VO2max and oxygen consumption by comparison with those on placebo, despite the fact that there were no significant changes in hematological measures.

Such findings are not restricted to endurance activities. A very recent six-week study examined the effects of tissue iron depletion on dynamic knee extensions in young women.(7) The participants, who all had low serum ferritin but normal hemoglobin levels, were treated with either iron or placebo. In the iron-supplemented group, the number of maximal voluntary contractions performed in a subsequent test was significantly higher than in the placebo group. These improvements did not seem to be related to measured changes in iron-status indexes or tissue iron stores. Interestingly, though, serum transferring receptor concentrations increased significantly in the placebo group, suggesting that they were suffering further iron depletion!

It has long been recognized that iron deficiency serious enough to lead to reduced blood hemoglobin also impairs aerobic performance and reduces VO2max; the function of hemoglobin is, after all, to transport oxygen to the working muscles. But how do more marginal iron deficiencies that are not accompanied by anemia affect performance? Although this type of iron deficiency is known to be commonplace in Western societies,(8) there has until recently been a poor understanding of how it impacts on physical performance.

Animal studies have indicated that endurance capacity and the effects of endurance training are diminished when a mild iron deficiency without anemia exists, and that this probably occurs as a result of diminished concentrations of iron dependent muscle enzymes and respiratory proteins involved in the biochemical pathways of aerobic metabolism.(9,10)

However, although many previous human studies have found suggestive relationships between mild iron deficiency without anemia and reduced aerobic performance, many of these findings have failed to reach statistical significance (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 bottom line is that most recent research clearly suggest that a ferritin (iron storage) deficiency—in the absence of anemia—will not only impair aerobic performance, but limit the adaptations that occur following aerobic training. In the light of this, it appears that maintaining an optimum iron status could be far more important for athletes than has previously been realized, especially given that even a mild shortfall appears to not only reduce maximum oxygen uptake capacity and aerobic efficiency but also to reduce the body’s response to aerobic training. The fact that iron is more difficult to absorb than most other nutrients and that vigorous aerobic training appears to readily deplete tissue iron only serves to underline the extent of the potential problem.

Testing for iron status is also far from straightforward. A low blood hemoglobin (Hb) measurement only appears in the very advanced stages of iron deficiency. One of the most functional, practical and economical is the ferritin iron finger stick, an at-home assessment available only at www.bioletics.com.

By this point in time, you may be convinced that you should be taking an iron supplement. But its important to know that starting yourself on a random, routine dose isn’t a good idea. Excess iron is not easily excreted. Self dosage on high-strength iron supplements for long periods of time can induce toxicity. In addition, Iron competes for uptake with several minerals in the body, especially copper and zinc; large doses of iron can therefore reduce the uptake of other important minerals, creating imbalances. Before you taken any iron supplement, make sure your iron status has been properly assessed.

Are you iron deficient? 

The following factors may increase your risk of developing an iron deficiency, particularly those marked with an asterisk:

• My sport involves significant volumes of running or other forms of endurance exercise*

• I am female

• I have regular periods*

• I have had children

• There is a history of anemia in my family

• I am vegetarian

• I am vegan*

• I drink tea and coffee with my meals*

• I use bran products

• I only eat white meat and fish (no red meat)

• I give blood regularly*

• I cook using aluminum or enamel cookware (not stainless steel or iron)

• I frequently take antibiotics, aspirin or antacids (indigestion remedies) 

Looking for ways to boost your dietary iron intake?

• If you’re not a vegetarian, make sure to include some lean cuts of grass-fed meat in your diet on a regular basis.

• If you are vegetarian, aim to consume more beans (especially lima beans), lentils, dark green leafy vegetables, eggs and nuts.

• Increase your intake of vitamin C-rich foods (including citrus fruits, berries, new potatoes, broccoli, sprouts, tomatoes, peppers and kiwis). Vitamin C helps convert Fe3+ in the body to Fe2+, making it up to four times more absorbable.

• Don’t drink tea and coffee with meals as the tannins they contain will strongly bind to any iron in food, making it less available to the body.

• Go easy on your consumption of pure bran as it is very high in phytates, which also bind iron. If you want more fiber in your diet, opt for a vegetable-based source (like salad greens).

• Use cast iron or stainless steel cookware, which can add useful amounts of iron to cooked foods.

 

References

1. Int J Sports Med, 23(8): 544-8, 2002

2. Med Sci Sports Exerc, 34(5): 869- 75, 2002

3. Physiol Behav, 75(1-2): 201-6 2002

4. Med Sci Sports Exerc, 25(5): 562- 71, 1993

5. Am J Clin Nutr, 66(2): 334-41, 1997

6. Med Sci Sports Exerc, 33(5): 741- 6, 2001

7. Am J Clin Nutr, 77(2): 441-8 2003

8. JAMA, 227:973- 6, 1997

9. J Clin Invest, 58:447-53, 1976

10. J Appl Physiol, 62:2442-6, 1987

11. Am J Clin Nutr, 75(4): 734-42, 2002

12. Am J Clin Nutr, 79(3): 437-43, 2004