Key words
iron supplement - intravenous iron - athlete - nutrient deficiency
Introduction
Iron deficiency is a common nutrient disorder in athletes, which left untreated, can
have significant impacts on training consistency and athletic performance.
Currently, there are a variety of methods that practitioners can use to address an
iron deficiency [1], with the appropriate approach
taken usually determined by the severity of the issue. Such approaches include
dietary assessment and food modulation (lowest severity), oral iron supplementation,
or parenteral iron delivery (highest severity). To determine the best approach, a
standardised process for establishing the severity of the issues must be first
considered.
Currently, there are numerous biological markers available to establish the iron
status of an athlete [2]; however, many of these
markers are acutely influenced by exercise, and a true gold standard of
measuring/reporting iron status in athlete populations is yet to be clearly
determined. Despite these issues, typical current practice sees iron status commonly
determined via the presenting iron stores (serum ferritin; sFer), transferrin
saturation (Tsat), and haemoglobin concentration (Hb). In combination, these three
blood markers are then typically used to categorise the
significance/severity of disrupted iron stores into three stages, as shown
in [Table 1], which provides a collective summary of
several published sources as a guide to help categorise an athlete’s iron
status [3]
[4]
[5]
[6]. Of note, the
interpretation of iron status from a single marker (i. e. only sFer) is not
recommended [7], and the impact of
exercise/training on these blood markers should be minimised using the
pre-blood screening guidelines established by Sim et al. [8].
Table 1 Classification, description, and common treatment
approach to various levels of iron status based on the presenting serum
ferritin (sFer), transferrin saturation (Tsat), and haemoglobin
(Hb).
|
Classification
|
Serum Ferritin
|
Transferrin Saturation
|
Haemoglobin
|
Description
|
Common treatment approach
|
|
Healthy iron status
|
>50 µg.L− 1
|
>16%
|
F:>120 g.L− 1
M:>130 g.L− 1
|
Iron stores and blood parameters are healthy
|
NA
|
|
Sub-optimal iron stores
|
35–50 µg.L− 1
|
Ferritin threshold of
50 µg.L− 1 is
associated with a hepcidin threshold for increased iron
absorption, signalling the onset of early ID
|
Nutritional assessment
|
|
Iron depletion (ID)
|
25–35 µg.L− 1
|
Iron stores in the bone marrow, liver, and spleen are
depleted
|
Nutritional assessment and potential oral iron supplement
|
|
Iron deficiency non-anaemia (IDNA)
|
15–25 µg.L− 1
|
<16%
|
Iron supply to the erythroid marrow is reduced
|
Nutritional assessment and oral iron supplement
|
|
Iron deficiency anaemia (IDA)
|
<15 µg.L− 1
|
F: <120 g.L− 1 M:
<130 g.L− 1
|
Haemoglobin concentration and oxygen-carrying capacity is
decreased
|
Parenteral iron
|
Note: F=female; M=male. Table created based on
combined data and explanations from [3]
[4]
[5]
[6].
Within athlete populations, it is commonly reported that the prevalence of iron
deficiency (anaemia (IDA) and non-anaemia (IDNA)) is 15–35% in
females and ~3–11% in males [8]
[9]
[10].
However, specific athlete cohort studies report>50% of a study
population can present with compromised iron stores [11]
[12]. Regarding the more severe stages
of iron deficiency (IDA), various studies inform a prevalence of
2–5% in females and 1–2% in males [13]
[14]. Across both
IDNA and IDA, the higher prevalence in females is generally attributed to the impact
of the menstrual cycle.
Given the high prevalence of iron deficiency in athlete populations, it is important
to understand the mechanisms of relevance that can collectively impact iron stores.
Currently, we understand that there are several mechanisms of iron loss during
exercise. These include processes such as haemolysis, sweating, haematuria, and
gastrointestinal blood loss [15]. Further, it is also
evident that athletes commonly battle energy deficit (through lack of time for
adequate recovery nutrition or through purposeful calorie restriction in
weight-sensitive sports), which can be associated with low nutrient quality and
inadequate iron intake from the diet [16]. Finally,
we also know that exercise results in a transient increase to the body’s
iron regulatory hormone, hepcidin [17], which results
in a temporary reduction in the absorption of iron from the gut, especially in foods
consumed 2 h post-exercise [18], where
absorption seems to coincide with the peak post-exercise elevations in hepcidin
levels at 3–6 h [17].
Although the iron loss from any single mechanism above might be small, it is their
combined effect over multiple training sessions that may accrue and present as a
burden on an athlete’s iron stores over time. Clearly, these mechanisms
present a case for iron loss during exercise, but equally, a period of reduced iron
absorption in the post-exercise period. Impacting the mechanisms of iron loss during
exercise is challenging, since there is limited ability for a practitioner, coach,
or athlete to control these factors when a certain type, duration, or intensity of
training is required for appropriate physical adaptation. However, our ability to
impact iron provision and uptake from the diet and/or from various methods
of supplementation, are very good. Therefore, a focus on timing iron intake to
coincide with peak periods of absorption (or to avoid peak periods of malabsorption)
from the gut becomes important, since it is the gut propensity for iron uptake that
limits our ability to effectively treat iron deficiency through food and oral iron
supplements.
Recent work from our group [1]
[12]
[19]
[20]
[21] and others
[18], have been exploring factors that impact
dietary iron absorption from the gut in relation to exercise. Collectively, this
work informs us that there appears to be a peak period for iron absorption within
the 30 min either side of exercise [19]
[21], which is lost if the food/supplement is
consumed≥2 h post-exercise [18].
Further, this propensity for increased absorption appears better in the morning as
compared to the afternoon [19], likely due to the
natural diurnal increase in hepcidin levels that marginally negates afternoon iron
absorption from a one-off meal [22]. Collectively,
this work provides us with significant strategic approaches to timing iron intake
for optimised iron absorption at the gut. However, if we are using these strategies
to correct an iron deficiency, it should be considered that the time duration to
have a significant impact is relatively long (i. e. 8–12 weeks of
oral supplementation to improve iron status by 40–80% [12]
[23]
[24]. Although this result is positive and appropriate
for individuals who are IDNA or better, an 80% improvement in iron stores
for an IDA athlete with sFer
<10 µg.L− 1 and compromised
Hb concentrations would likely still not shift them into the IDNA classification.
Accordingly, contemporary approaches to iron replenishment in these specific IDA
athlete populations are focussed on parenteral iron provision, which has the benefit
of by-passing the gut (where our key limitations exist) and supplying iron direct to
circulation. Regardless, the use case for such approaches should be well considered
by the practitioner and athlete, and therefore, the remainder of this review will
focus on parenteral iron delivery in athletes.
Parenteral iron approaches to treating anaemia
Parenteral iron approaches to treating anaemia
Parenteral treatment of iron deficiency is particularly warranted in the presence of
severe IDA, or when there are ongoing and significant iron losses (e. g.
heavy menstrual bleeding) [25]. Of note, thorough
investigation of the underlying cause and exclusion of medical conditions such as
occult gastrointestinal (GI) blood loss (e. g., from non-steroidal
anti-inflammatory use, carcinoma), malabsorption (e. g. coeliac disease),
and non-GI blood loss (e. g. abnormal uterine bleeding), should be
considered by the treating physician [26].
Unsurprisingly, in clinical populations with chronically elevated hepcidin levels
(e. g. cancer, inflammatory conditions), parenteral iron administration is
recommended as it overcomes the negative effect of hepcidin on GI absorption [27]. In athletes, where repeated exercise-induced
elevations of hepcidin occur daily [17]
[28], the limitations to gut absorption of oral iron
intake may be substantial. Interestingly, the amount of hepcidin required to block
iron absorption from the gut is lower than that required to block iron recycling
from macrophages, where intravenous (IV) iron is taken up [29]. Therefore, parenteral iron therapy becomes a viable treatment option
for athletes presenting with IDA, or in those presenting with an inadequate
response, intolerable side-effects, or poor adherence to oral iron therapy [25].
Intravenous iron: formulations and safety
Intravenous iron: formulations and safety
Intravenous (IV) iron consists of an iron core within a carbohydrate shell [29]. The stability of the shell dictates the maximum
dose that can be given in a single infusion: iron sucrose is less stable, allowing
for only 200 mg to be administered per infusion [29], whereas the newer formulations of ferric carboxymaltose, ferric
derisomaltose, low molecular weight iron dextran, and ferumoxytol have stable
shells, permitting larger doses and fewer total infusions [25]
[30]. Ferric derisomaltose and
ferumoxytol, for example, are typically provided in a single infusion of up to
1000 mg over 15 min, in contrast to the multiple infusions required
with iron sucrose [31]. Iron polymaltose is a cheaper
preparation, which is also approved for total dose infusion, although over a longer
period by slow infusion (~ 5 h) [32]
[33]; more rapid infusion (~
1 h) of iron polymaltose, however, may be safe and well-tolerated [33]
[34]. The cumulative
dose required is based on the individual’s Hb, target Hb, and body weight
[32], although some centres adopt a
‘standard’ 1-g dose protocol [35].
While serious adverse events and infusion reactions (e. g. anaphylaxis) were
previously a concern with early IV preparations, primarily due to high molecular
weight iron dextran formulations that are no longer available [36]
[37], the newer
formulations appear to have a similar safety profile to oral iron [31]. In fact, a meta-analysis from 2015 (n=103
randomised controlled trials) reported no increased risk of serious adverse events
(relative risk 1.04 95%CI 0.93–1.17), compared to oral iron or
placebo [38]. Milder reactions, such as headache,
fever, joint pain, and urticaria, however, might be expected [25]
[39]. Nevertheless,
monitoring for 30 min after infusion by appropriately qualified staff is
still advised [25] to monitor for and manage severe
reactions (e. g. loss of consciousness, cardiac arrest,
wheezing/stridor, hypotension) [39].
Iron-induced hypophosphatemia can occur following IV iron, particularly with ferric
carboxymaltose, however is usually transient and frequently asymptomatic [31]. Nevertheless, phosphate measurement and
replacement must be considered in individuals presenting with symptoms, such as
muscle weakness and mental state changes, following parenteral iron treatment [25]. In the case of repeated administration, bone pain
and fractures may also alert the clinician to possible hypophosphatemia [25] a risk that should also be considered and
discussed prior to administration in athletes.
Intramuscular iron
Intramuscular (IM) iron, while effective, has shown to be no safer than intravenous
(IV) iron, can be more painful, and is associated with permanent skin staining and
possibly sarcomas [26]
[27]
[32]
[33]. For athletes, this would be especially problematic as it has the
potential to negatively impact training or competition in the immediate days
post-treatment. Notably, current best practice guidelines from the Australian
Institute of Sport (AIS) indicate a preference for IV iron infusion (preferably
ferric carboxymaltose) only in athletes presenting with severe IDA, ineffective oral
supplementation, or compromised Hbmass in close proximity to a major
sporting event [40]. Most importantly, both IV and IM
iron therapy must be guided by sports physicians in-conjunction with a particular
organisations policy (e. g. no needle).
Efficacy of IV formulations on haematological variables
Efficacy of IV formulations on haematological variables
Advantageously, newer IV formulations allow for complete, or almost complete, iron
repletion to occur with a single dose (~1000 mg) administered over
15–60 min [31]. With these total dose
protocols, peak ferritin concentrations are achieved in 7–9 days [41] with pharmacokinetic studies (using lower doses of
200 mg) demonstrating persistent elevations compared to baseline at 2 weeks
[42]. The incremental increase in Hb varies
depending on the initial Hb and the dose given [43].
Current evidence in clinical populations suggests that Hb increases by
2 g.dL− 1 per week; plateauing around
5–14 days [44]
[45]. Here, the significant advantage of IV formulations is highlighted by
the rapid normalisation of haematological parameters when compared to oral therapy.
Indeed, in IDA pregnant women (mean sFer: 13
μg.L− 1, Hb
11.4 g.dL− 1), IV iron (1000 mg of
ferric carboxymaltose or iron polymaltose) resulted in larger sFer and Hb increases
at 4 weeks post infusion when compared to oral supplementation (325 mg daily
ferrous sulphate) [46]. Similarly, a study in IDA
postpartum women (sFer<15 μg.L− 1,
Hb<9 g.dL− 1) also demonstrated that
those treated with IV iron (iron sucrose 200 mg x 2) had more rapid
increases in Hb in the first 2 weeks than those receiving oral supplementation
(ferrous sulphate 200 mg twice daily) [45].
However, there was no significant difference between groups in Hb concentration at 6
weeks [45], emphasising that, where GI absorption is
not impaired, similar longer-term outcomes can be achieved with oral and IV routes.
Nevertheless, the rapidity of repletion and the ability to circumvent the gut is
particularly attractive in certain clinical populations, including IDA athletes.
A target increase in Hb of ~ 2 g.dL− 1 at
2–4 weeks is recommended in medical guidelines [47], with subsequent measurement of Hb at 4 weeks (or earlier if
symptomatic), to evaluate treatment response and decide on subsequent doses [47]. Here, it is worth noting that, in athletes, the
measurement of Hb to monitor the response to iron therapy in anaemia may be
misleading. Haemoglobin concentration is dependent upon both the absolute mass of
haemoglobin (i. e. Hbmass) and blood volume (plasma and red
cells) [48]. In athletes, Hb may be falsely low due
to increased plasma volume or falsely high in the setting of dehydration. Therefore,
the use of Hbmass (through carbon monoxide rebreathing technique [49]) may be more precise and provide better
information about oxygen carrying capacity. Nevertheless, this measurement is
generally confined to research situations and is difficult for clinical practice.
Accordingly, practitioners and clinicians are advised to employ current best
practice standardisation protocols (e. g. well-hydrated state, morning
sample, body position, rested and limited exercise in the 12 h prior to
sampling) to maximise the validity and reliability of venous blood measurements
[8].
Impact of parenteral iron approaches in athletes
Impact of parenteral iron approaches in athletes
Efficacy of parenteral iron on performance outcomes in non-anaemic
athletes
While studies in athletes are limited, the effect of IV iron on haematological
and performance indices appears to be dependent on the severity of iron
deficiency pre-infusion. Burden and colleagues [50] examined the short- and medium-term effects of a 500 mg
IV iron infusion in highly trained IDNA female (sFer <30
μg.L− 1,
Hb>12 g.dL− 1) and male (sFer
<40 μg.L− 1,
Hb>12 g.dL− 1) marathon runners
(Tsat 33.1±12.0%). Twenty-four hours after the infusion, mean
sFer concentrations increased and remained elevated 4 weeks later. However, no
differences in Hb concentrations, running economy, time to exhaustion, or
VO2max were reported at either 24 h or 4 weeks
post-infusion. Further, a randomized controlled trial by Woods and colleagues
[51] recruited 14 distance runners without
iron deficiency anaemia (sFer: 30–100
μg.L− 1,
Hb>12.0 g.dL− 1), and examined
the impact of three 100-mg IV iron (or placebo) treatments, each separated by 2
weeks, on performance, fatigue, and haematological indices. After 6 weeks,
improvements in fatigue (Cohen’s effect size –1.54,
p=0.05) and mood scores (Cohen’s effect size –1.58,
p=0.02) were reported in the group receiving IV iron, in contrast to the
group receiving a saline placebo injection. Unsurprisingly, no improvement in
3000-m time-trial performance was seen at week 4 nor was there any increase in
Hbmass at week 6 post-infusion [51], outcomes likely explained by the relatively high iron stores of
the athletes (sFer>30 μg.L− 1) prior
to infusion.
In addition to these findings, Garvican and colleagues [24] examined the efficacy of IV ferric carboxymaltose in highly
trained distance runners with low (sFer≤35
μg.L− 1 and Tsat<20%, or
sFer≤15 μg.L− 1) or sub-optimal iron
stores (sFer <65 μg.L− 1). After a
series of IV injections over a 6-week period, Hbmass (4.9%) increased
only in the low iron stores group, which was accompanied by an increase in
VO2max (3.3%) and run time to exhaustion (9.3%).
Conversely, no change reported in the suboptimal group, suggesting that
supplementation is more effective when iron stores are compromised. Of interest,
an oral iron supplement group in the same study showed no increase in
Hbmass or VO2max after 6 weeks, regardless of initial
sFer status (low or suboptimal).
To summarise, it appears that iron supplementation in non-iron-deficient athletes
does not improve performance, and therefore, indiscriminate use of IV iron is
not recommended. However, greater efficacy of IV iron supplementation is
observed in athletes with lower sFer concentrations, suggesting the practice
should be reserved for cases where iron stores are significantly compromised,
such as IDA.
Efficacy of parenteral iron on performance outcomes in anaemic
athletes
Few studies have investigated the effect of parenteral iron on haematological and
performance variables in IDA athletes. A single case report has been published
on a female athlete with IDA and represents the only
‘longitudinal’ (15 weeks) evidence for parenteral approaches to
be used with anaemic athletes. Here, a female middle-distance runner (sFer 9.9
μg.L− 1, Hb
8.8 g.L− 1) received an IM iron injection
(100 mg Fe), which was followed by 15 weeks of oral iron supplementation
[52]. After 2 weeks, initial improvements in
haematological variables were rapid, where the authors describe a 136%
increase in sFer (to 23.4 μg.L− 1),
36% increase in Hb (to 12 g.dL− 1)
and a 49% increase in Hbmass (389 g to
580 g). These outcomes were maintained, if not improved, at 15 weeks
post-injection (sFer 27.0 μg.L− 1, Hb
13 g.dL− 1 and Hbmass 710 g).
Alongside the haematological improvements, the athlete ran a personal best time
over 3,000 m ~70 days post-infusion. Although this case study
showed a rapid and prolonged effectiveness of parental treatment in a single
athlete, it should be noted that this approach was combined with oral iron
supplementation, making it difficult to distinguish the sole efficacy of IM
injections. Similarly, Pedlar et al., [7] showed
IM iron injections given to a female Olympic Games 1500-m runner increased sFer
levels more than four-fold (from 11 μg.L− 1
to 47 μg.L− 1; extrapolated from Figure 1 in
Pedlar et al. [7]) prior to a major event.
However, these improved iron stores were back down to similar pre-IM injection
levels within 6 months, despite oral iron supplements being used to support the
increase. Of note, the athlete presented in the study by Pedlar and colleagues
was not considered to have IDA (with Hb
levels>120 g.L− 1), and
therefore, no study has to date examined the long-term effects of parenteral
iron treatments in elite athletes with IDA, and the impact this may have on
performance. Accordingly, much needed research in this space is required to
better inform practitioners of the potential benefits of parenteral iron
treatment.
Long-term impacts and decay
In a retrospective examination of a highly trained female athlete cohort with
IDNA, McKay et al. [53] modelled the rate of
decay in sFer following an IV infusion. These authors reported that sFer takes
499 days [range: 212–776 days] and 647 days [361–925 days]
post-infusion to fall to 50 μg.L− 1and 35
μg.L− 1, respectively. Importantly, each
individual athlete responded differently, with a random intercept for
“subject” accounting for the majority of model variance, and
factors such as the athletes’ sport, age, or pre-infusion ferritin
concentrations deemed less important. Noteworthily, potential confounding
factors such as training load, menstrual cycle status, and dietary intake were
not considered and may significantly contribute to the rate of sFer decay.
Nevertheless, current recommendations suggest that athletes undergoing an IV
iron infusion should assess iron status 1 month post-infusion to determine
treatment efficacy, with a repeat assessment at 6 months post-infusion to
determine iron retention [53]. If further
follow-up treatment is required, this should be developed on an individual basis
and may include a combination of dietary, oral, and parenteral strategies;
although, as noted above, sFer levels still decayed to baseline by 6 months
post-IM injection in the case study presented by Pedlar et al., [7] despite being supported with oral iron
supplements during this period, which further highlights the individual response
to treatment. Accordingly, future research should examine the rate of decay in
sFer and Hb prospectively, considering differences between IDA and IDNA
athletes, as well as the potential influence of individual factors which may
affect the rate of decay.
Special considerations of parenteral iron use in athletes
Special considerations of parenteral iron use in athletes
World Anti-Doping Code Considerations
For athletes engaging in international competition, consideration must be given
to the regulations governing the use of IV infusions. The World Anti-Doping
Agency (WADA) defines an IV infusion as ‘the supply of fluid
and/or prescribed medication by drip or push directly into a
vein’ and states that they are ‘prohibited both in-competition
and out-of-competition if the volume delivered exceeds 100 ml within a
12-h period’ [54]. However, if the
infusion is received in the course of hospital treatment, a surgical procedure,
or clinical diagnostic investigations, a therapeutic use exemption (TUE) may be
necessary [54]. Although formulations vary in how
they are administered (injection versus infusion, volume of solution), iron
polymaltose, given as a slow infusion, typically exceeds this volume, and
therefore, preference may be given to formulations such as ferric
carboxymaltose. As such, consideration must be given to the need for IV therapy,
the formulation used, and in some cases, potential application for a TUE prior
to administration of IV iron in athlete populations.
Altitude
Unique to athletes is the need to consider iron supplementation prospectively to
defend against the anticipated increased iron demand for physiological
adaptation. Altitude training is frequently utilized by endurance athletes with
the aim of inducing hypoxia-mediated adaptations to erythropoiesis.
Supplementary iron is recommended when sFer is less than 35
μg.L− 1 at 4–6 weeks prior,
or<130 μg.L− 1 at 2 weeks prior to
altitude, in an attempt to optimize increases in Hbmass
[55]. Unless sFer is less than 15
μg.L− 1, oral iron is preferred to align
with the “no needle” policies of many sporting organizations
[55]. Indeed, a study in non-anaemic
endurance-trained athletes (Hb ~
14 g.dL− 1; mean sFer ~
71.2–88.1 μg.L− 1 with 4 of 34
subjects with sFer<20 ug.L− 1), demonstrated
a similar increase in Hbmass after 21 days of simulated altitude
exposure in both oral (3.7%) and IV (3.2%) iron-supplemented
groups, in contrast to a lack of Hbmass response in the placebo group
(0.1%) [56]. This was associated with a
larger increase in sFer in the 2 weeks prior to altitude exposure in the IV
group, compared to the oral and placebo groups (IV 47% and 92%
larger, respectively), and an increase in VO2peak after altitude in
the IV supplemented group only. Of note, a decrease in VO2peak was
seen in individuals across all groups, leading the authors to postulate that the
results may have been confounded by residual fatigue after altitude training
[56]. This study, combined with the
guidelines presented above, suggest that iron supplementation might be necessary
for hypoxia-mediated erythropoietic adaptation even in non-iron deficient
athletes. Further, IV supplementation does not provide additional benefit to
Hbmass over oral therapy in non-iron deficient athletes [56]. However, considering the time required for IV
iron to impact ferritin and Hb over oral iron supplementation in the short term
(1–4 weeks), IV iron may be necessary in an IDA or IDNA athlete where a
rapid rate of increase is required due to a limited lead-up time to altitude
exposure.
Pregnancy
Pregnant women are a special population requiring consideration, with the
increased numbers of athletes continuing sport throughout pregnancy. Indeed, IDA
affects ~37% of pregnant women (aged 15–49 years)
worldwide [57], and when considering the
increased iron requirements needed to simultaneously support both foetal
development and high training loads, it is unsurprising that pregnant athletes
are an extremely high risk group for iron deficiency. Pregnant athletes are a
severely under-researched population, and so, current guidance is limited. Iron
deficiency in pregnancy is known to have potential adverse maternal and foetal
outcomes, such as premature birth, low birth weight, maternal infections, and
increased maternal mortality [57]. Where
treatment is required, oral iron is the first line approach, with IV iron
indicated only if the response to oral therapy is inadequate and only in the
second and third trimesters [31]
[58]. However, given the adverse GI side-effects
from oral therapy, there is increased interest in newer IV preparations. Indeed,
a recent meta-analysis suggested an increased rate of target Hb achievement
(OR=2.66), increased Hb after 4 weeks
(WMD=0.84 g.dL− 1), and decreased
adverse reactions (OR=0.35) in pregnant women receiving IV compared to
oral iron supplementation [59]. Additionally,
ferric carboxymaltose may have fewer side-effects while also being more
convenient and less costly than iron sucrose [60]. In pregnant athletes, where the risk of iron deficiency may be
amplified, the use of IV iron could be preferable; however, further research,
particularly on long-term outcomes, is warranted.
Summary and conclusions
The high prevalence of iron deficiency in athletes is attributed to a combination of
increased losses, inadequate dietary intake, and exercise-induced increases in
hepcidin. While oral iron supplementation is considered first-line treatment, the
significant adverse GI side effects and the need to optimally time consumption
around exercise pose potential challenges in the adherence and absorption of iron
orally administered in athletes. On the other hand, parenteral iron, specifically
IV, offers the advantage of circumventing hepcidin inhibition in the GI tract, while
achieving more rapid increases in sFer and Hb. Of note, newer IV formulations allow
for single total dose administration within an hour with a similar safety profile to
that of oral iron. Current evidence suggests notable improvements with IV iron
therapy in haematological and performance variables in IDA, and in IDNA where sFer
is<15 μg.L− 1. However, it is
understandable that various sporting organisations have a cautious approach to the
use of needles for treating nutrient deficiencies, confining IV iron therapy to IDA,
ineffective long-term oral supplementation, or compromised haematological status in
close proximity to a major sporting event [40]. In
addition, parenteral iron should only be administered in consultation with a sports
medicine physician, where consideration must be given to the need for a TUE in
accordance with WADA regulations. Finally, future studies investigating parenteral
iron approaches in athletes are warranted to assess the longer-term impacts on
haematological and performance variables, in addition to exploring the individual
factors (e. g. training load, dietary intake, menstrual cycle status) that
affect the rate of decay.
