A friend of mine alerted me to this super useful review on iron deficiency in athletes, however it is going to be one for anyone who has struggled with low iron status, athlete or not. I’ve summarised the main points and recommendations below.
How prevalent is iron deficiency in the athletic population?
Although iron deficiency is most common in female athletes (~15–35% athlete cohorts deficient), approximately 5–11% of male athlete cohorts also present with this issue. For obvious reasons, potentially a result of increased iron demand to account for menses. However, low energy intake, vegetarian diets and endurance exercise have also been proposed as potential factors impacting both male and female athletes’ iron stores
How would you know?
The symptoms of compromised iron status include lethargy, fatigue and negative mood states with more severe cases (i.e. iron deficiency anaemia; IDA) also compromising work capacity. Such symptoms may impact the athlete’s ability to train appropriately and to produce competitive performances.
Getting blood tests – what to look for?
Stage 1—iron deficiency (ID): ferritin <15 g/L, transferrin saturation>16%
Stage 2—iron-deficient non-anaemia (IDNA): ferritin<15 g/L, transferrin saturation < 12μg/L
Stage 3—iron-deficient anaemia (IDA): Haemoglobin (Hb) production falls, resulting in anaemia (ferritin < 12μg/L, Hb. Additionally, serum-soluble transferrin receptor (sTfR) levels of 2.5 mg/L could be considered a reasonable threshold for identification of IDA.
How does training affect what you see in blood test results?
Well it can, is that just using ferritin as a marker of iron status may not be a good idea as it is an acute phase protein, and the fact that ferritin levels are increased during periods of inflammation and after intensive exercise. Furthermore, measures of Hb are also affected by shifts in plasma volume, which, when unaccounted for, may present issues such as pseudo-anaemia or sports anaemia which does not appear to have any negative effects on performance. Considering training and/or heat adaptions can induce hypervolaemia these factors should be considered to avoid diagnosing deficiency that isn’t there.
What causes Iron deficiency?
- haemolysis exacerbated by ground impact forces (e.g. foot strike) and
- muscle contraction (e.g. eccentric muscle damaging exercise)
- gastro-intestinal (GI) bleeding,
- heavy menstrual losses and
- inflammatory/iron regulatory hormone (hepcidin) responses exercise has a transient impact on increasing levels of the master iron regulatory hormone, hepcidin (for 3–6 h post-exercise), likely a result of the well-documented exercise-induced inflammatory response and associated increases in the cytokine interleukin-6 (IL-6) Increases in hepcidin activity result in a decrease in iron absorption and recycling from the gut and scavenging macrophages, respectively. As such, it is likely that there exists a transient window of altered iron metabolism after exercise where nutrition strategies could be exploited to manipulate the outcome (i.e. strategic feeding times to avoid the window of decreased iron absorption). It’s tricky given how often athletes train, combined with the fact it’s lower in morning and rises during the day – however if you eat cereal in AM, this will impair absorption. Appears to be a window of an hour post-training where you can maximise iron absorption – before hepcidin rises too much. This increase happens in all athletes too, IDA or not. So best time for supplementation could be 60 min post exercise in AM after breakfast, using iron enhancers (vit C, acetic acid – apple cider vinegar) and not drinking coffee or tea or consuming too much calcium which will compete with iron for uptake into the cells.
- Both testosterone and oestrogen can influence iron metabolism via their suppressive effects on the hepcidin–ferroportin axis For athletes, it is possible that high training loads may alter an individual’s hormonal profile thereby suppressing gonadotropin-releasing hormone (GnRH), a precursor for sex hormones. In women, this can lead to suppressed luteinising hormone (LH), follicle stimulating hormone (FSH; to a lesser extent) and consequently oestrogen. Low oestrogen, less suppression of hepcidin, so higher levels impact on absorption.
- Consequently, chronic suppression of testosterone may be linked to higher hepcidin levels in male athletes, potentially impairing iron regulation, and thereby helping to explain the incidence of ID among this sex, especially as endurance athletes often have lower testosterone. In women, although lower levels of testosterone are present, its importance in iron metabolism should not be ignored. For example, higher testosterone levels have been associated with lower risk for anaemia in both healthy older women (n=509) and men (n=396)
How effective is supplementation?
It doesn’t give a performance boost if not deficient, however requirements may be greater, as studies have shown that 30-40% losses ferritin over a harder training block, so the typical 13-18mg / day recommended is probably not enough. Some researchers think that training adaptations typically associated with endurance training may only be maximised in the presence of adequate iron stores.
Does diet matter?
Outside of the obvious limitations that a vegetarian or vegan diet present with (low available iron that requires supplementation) a lower CHO availability (depleted glycogen stores) may increase inflammatory markers like IL6 and hepcidin which can impact on absorption – this has been found transiently but may not be a problem over the long term in presence of higher muscle glycogen and a higher protein intake. More research is needed in the area of CHO availability and iron status.
How to ensure adequate iron status?
Strategy: check at risk athletes every three months, getting bloods in a fasted, rested state with no hard workout in the 48 hours prior (and ideally no injury present). Also, monitor diet via an app to check overall intake through diet (red meat, organ meat and mussels are the best dietary sources, we are able to absorb 20% of available iron from these compared to 5% from vegetarian diets).
Take supplements – ones which are easy on the gut – the commonly prescribed ferrograd is not. Thorne iron biglycinate, Spa tone and Carbonyl iron are three which are better tolerated. Generally, the overall response to oral iron supplementation in athlete cohorts appears positive (40–80% increases to ferritin) when consumed over an 8- to 12-week time frame. In addition, alternate day supplementation may increase the efficacy of effect via an improvement in the absorption of iron from a given dose, which, over time, results in a greater cumulative response (Stofel et al. 2017). Such regimens, in combination with iron absorption enhancers such as vitamin C.
With this in mind, IV infusion may be a better option when levels are super low and a situation requires rapid improvement in iron stores, or when gut issues appear to render supplementation ineffective.
Also it is worth considering is the concept of maximising iron stores through supplementation during periods of lower activity (e.g. of-season). Inevitably, as training load and iron demands increase during the competitive season, higher iron reserves may limit the negative influence that exercise training has on the bioavailability of iron.