No, this isn't another article about the classic 1989 Dave Scott vs. Mark Allen Hawaii Ironman epic!

This article focuses on that important mineral "iron" central to endurance performance.

Running the human performance lab up here at Wesley Corporate Health is always an interesting education in putting theory into practice. Of late, we have had a spate of young female distance runners coming through the Peak Performance Lab to be assessed for VO2max, biomechanics, body composition and anaerobic threshold. As a standard part of our assessment procedures all athletes through the Peak Performance Lab complete an FBT - full blood test - and one of the parameters I have reviewed is serum ferritin. Why serum ferritin? Lowered levels of serum ferritin are an indicator of compromised iron stores, in fact a much better indicator in athletes than simply reviewing red cell mass and the like, as endurance athletes tend to experience a plasma volume expansion which, when looking at standard makers of anemia (other than serum ferritin), can be misleading.

Of interest has been the fact that many of these young athletes that have been coming through the lab have been, technically speaking, anemic. All were complaining of feelings of lethargy - feeling, flat, no energy, etc. and when tested on the treadmill, to a person, their lactate velocity curves were very "steep" indicating that very quickly their bodies were producing lactic acid faster than they could clear it. This is a sure sign that aerobic metabolism has been lowered and that the athletes are quickly starting to rely on anaerobic metabolism to take up the slack (i.e. Aerobic metabolism relies on the transportation of oxygen around the body which is bound to the hemoglobin component of red blood cells. The major constituent of hemoglobin is iron, so once iron stores have been comprised the body doesn't transport oxygen as effectively sending it anaerobic quicker and hence lowering endurance performance).

The prevalence of iron deficiency anemia is likely to be higher in athletic populations and groups, especially in younger female athletes, than in healthy sedentary individuals. In anemic individuals, iron deficiency often not only decreases athletic performance but also impairs immune function and leads to other physiologic dysfunction. Although it is likely that dietary choices explain much of a negative iron balance, evidence also exists for increased rates of red cell iron and whole-body iron turnover in endurance athletes.

Research has suggested that endurance athletes, especially distance runners, have higher iron turnover rates because of various factors including:

1. "Heel strike hemolysis" - every-time your foot hits the ground red blood cells are squashed between the heel and the ground increasing iron turnover.

2. Sweat loss in heavily sweating athletes.

3. Micro trauma. When you run your gastrointestinal tract "jiggles" - this causes small tears which bleed adding to iron losses.

4. Dietary choices (e.g. Choosing poor, iron deficient foods and/or combining inappropriate food choices which compete with iron for absorption).

5. In female athletes - menses. Blood loss as a consequence of the menstrual cycle.

So should all endurance athletes be taking an iron supplement?

No!

Iron overload can be toxic and in high enough concentrations lethal.

There are effectively two types of iron that humans consume: (i) "Heme" iron - generally derived from animal sources and (ii) "Non-heme" iron - generally derived from plant sources. Given that non heme iron has a lower "bioavailability" (absorption) it isn't surprising that vegetarian athletes often have jeopardised iron status. The role of heme and non-heme iron in biological function and work performance has been elucidated through various human and animal experiments. Several scientific review articles have been published over the years. As discussed above, hemoglobin iron, when lacking, can profoundly alter physical work performance via a decrease in oxygen transport to exercising muscle. What is intriguing, however, is that although non-heme iron associated with enzyme systems constitutes only 1% of total body iron, profound deficits of these cellular enzymes per se may have detrimental effects on athletic performance. Studies illustrate that maximal oxygen uptake (O2max) is determined primarily by the oxygen-carrying capacity of the blood and is thus correlated with the degree of anemia. Endurance performance at reduced exercise intensities, however, is more closely related to tissue iron concentrations because of the strong association between the ability to maintain prolonged sub-maximal exercise and the activity of iron-dependent oxidative enzymes located in the " aerobic energy production houses" of the body's cells - the mitochondria.

In severe anemia, oxygen transport limits aerobic function at any exercise intensity despite the blood "giving up" the available oxygen more effectively (O2 dissociation) and increased blood circulation (cardiac output). Oxygen uptake at a cellular level - in severe anemic conditions - can also be jeopardised due to lowered "myoglobin" levels - the binding site for oxygen on the cells - which are also iron dependent.

In short, lowered iron status has a cascading effect throughout the aerobic metabolism chain that conspires to lower an athletes' aerobic (and hence performance) capacity.

Given that blanket dietary supplementation ISN'T recommended for all endurance athletes what should be done?

First up, identify if you fall into one of the "at risk" groups. Are you:

1. A female distance-runner/triathlete.

2. Are you a vegetarian.

If you're a female triathlete/runner who consumes a vegetarian diet, you in particular are at risk!

If you've established that you are in one of these at risk groups then you'll need to:

a. Ensure that you are consuming the R.D.I. (recommended daily intake) for iron: Men = 7mg/day, women = 12-16mg/day.

b. Monitor your dietary intake.

c. Get some good nutritional counselling (e.g. Combining vitamin C intake with non-heme iron consumption improves iron absorption, avoiding calcium, caffeine and consumption of tannin-rich foods such as tea, wine, grapes at the same time as iron intake improves iron bioavailability).

d. DO NOT self medicate - only take a dietary iron supplement if directed to do so by a health professional such as a doctor or dietician and then serum ferritin status should be reviewed within 6-8 weeks to see if iron status has stabilized. In people who are genetically predisposed to iron imbalance, hemochromatosis (iron accumulation) may develop after prolonged iron supplementation and this can cause a raft of problems with the liver and brain and may even result in death. Therefore, minimal short term doses of supplemental iron are recommended (under medical supervision) to avoid a possible accumulation of this mineral.

In summary, it is clear that lowered iron status can reduce VO2max. Every attempt should be made to normalise iron status via "conventional" dietary and lifestyle methods. If this fails then supplementation under medical supervision is an option.