Iron deficiency, supplementation, and sports performance in female athletes: A systematic review

Highlights

• •High-level iron deficient female athlete can experience a negative impact on endurance performance, managed by supplementing with 100 mg of elemental iron per day or bi-daily.
• •Decrements in maximal aerobic capacity appear to coincide with the severity of iron deficiency.
• •Energy efficiency, maximal work rates/ velocities, and blood lactate may be enhanced by consuming 16–60 mg of elemental iron delivered daily for a duration of 42–56 days.
• •Iron deficient female athletes are encouraged to consult a sports medicine practitioner or sports dietitian to limit compromises in training and competitions while also ensuring iron supplementation protocols adhere with anti-doping guidelines.

Abstract

Background

Iron facilitates key biological functions underpinning sports performance, and up to 60% of female athletes experience iron deficiency. However, the effects of iron deficiency on sports performance in female athletes is unclear, as are the degree of benefits of iron supplementation (FeSup). This study characterizes the effects of iron deficiency and FeSup on sports performance in high-level female athletes.

Methods

Searches of the electronic databases MEDLINE, SPORTDiscus, Web of Science, Scopus, and CINAHL were performed in July 2023. Studies were included that evaluated the effects of iron deficiency or FeSup on sports performance in high-level (maximal oxygen uptake (VO_2max) > 45 mL/kg/min, or trained > 5 h/week) iron deficient (ID) (serum ferritin (sFer) < 40 µg/L) female athletes. Studies were assessed using a modified Downs and Black Quality Assessment Checklist.

Results

A total of 23 studies comprising 669 athletes (age range: 13–47 years) across 16 sports were included in the review. Iron deficiency negatively affects endurance performance by 3%–4%. However, endurance performance improved by 2%–20% when ID athletes were treated with 100 mg/day of elemental iron for up to 56 days via oral supplementation, or bi-daily via parenteral administration over 8–10 days. ID non-anemic athletes with low sFer stores may be predisposed to reduced maximal aerobic capacity. However, maximal aerobic capacity improved by 6%–15% following 16 mg/day–100 mg/day of elemental iron for 36–126 days. Isokinetic strength and anaerobic power performance may be impeded (–23% to +4%) among ID athletes, but the effect of FeSup on anaerobic power varied markedly (–5% to +9%) following 100 mg/day of elemental iron over 42–56 days, or 100 mg of elemental iron bi-daily over 8–10 days. The quality of studies was moderate (77%), ranging from low (57%) to high (100%). Moststudies (n = 18) contained group sizes ≤ 20 athletes, thus limiting the likelihood of detecting significant effects (statistical power > 0.80).

Conclusion

High-level ID female athletes experience a negative impact on endurance performance, which can be improved by supplementing with ∼100 mg of elemental iron per day or bi-daily. The decrements in other performance parameters characterizing a range of sports coincide with the severity of iron deficiency.

Graphical abstract

1. Introduction

Peak sports performance in athletes depends on various endogenous and exogenous physical, technical, mental, and tactical factors. However, adverse environmental, lifestyle, psychological, or physiological effects may lead to undesirable training and competitive results. Iron supports key biological functions for peak sports performance through erythropoiesis, oxygen transportation and uptake, and oxidative phosphorylation in the electron transport chain. Anecdotally, some athletes with iron deficiency appear to train and compete successfully, while others show impaired performance.1, 2, 3

Iron deficiency ranges from Stage 1 non-anemic iron deficiency (IDNA-1) to Stage 3 anemic iron deficiency (IDA-3); each stage is likely to elicit different effects on sports performance. IDA-3 is characterized by impaired erythropoiesis, compromising oxygen delivery via reductions in hemoglobin (Hb) concentration (<120 g/L).^4,5 When Hb concentration is deemed normal (Hb ≥ 120 g/L) but iron status is compromised, marked by reductions in serum ferritin (sFer) or transferrin saturation (TSAT), the individual is diagnosed with either IDNA-1 (sFer < 30 µg/L and TSAT >16%) or Stage 2 non-anemic iron deficiency (IDNA-2) (sFer < 20 µg/L and TSAT < 16%).^6,7 It appears there are other mechanisms affecting performance in IDNA-1 and -2 athletes when Hb concentration is not compromised.

Low ferritin levels, reflecting total body iron stores, are proposed to be the primary mechanism for increased fatigue and deficits in sports performance, even when Hb levels are normal.⁸ Low iron stores negatively affect oxidative enzymes, respiratory proteins, and cytochrome activity, impairing the extraction and utilization of oxygen for adenosine triphosphate (ATP) production.⁹ The impaired structure of these proteins limits oxygen transport within the electron transport chain, providing a mechanism whereby sports performance is compromised in athletes with IDNA-1 and -2. Despite efforts to standardize diagnostic criteria for iron deficiency in athletic cohorts, there is little consensus.¹⁰ Higher hematological biomarker cut-off values (e.g., sFer > 30 µg/L) may be required when determining iron deficiency in athletes with naturally greater iron losses. Without consensus on diagnostic criterion for determining iron deficiency, a combination of iron status, athlete's performance level, sex, training status, and sport may better indicate athletes who are susceptible to performance decrements.

Despite the importance of iron, iron deficiency remains highly prevalent, ranging globally between 9%¹¹ and 60%¹² in female athletes. The greater prevalence observed in female athletes compared to their male counterparts (typically up to 30%) is partly attributable to diet and menstruation, where eumenorrheic females can lose up to ∼10 mg of iron per menstrual cycle.¹³ Consequently, female athletes may experience issues, including menstrual irregularities, with implications on bone health.¹⁴ However, several strategies can be employed to treat diagnosed iron deficiency.

To support female athletes’ higher recommended dietary intake, iron is available in many supplemental forms. Hematological biomarkers have successfully responded to iron supplementation (FeSup) in iron deficient (ID) athletic cohorts.^15,16 However, the effectiveness of FeSup on physical parameters beyond endurance performance and maximal aerobic capacity is unclear, particularly in sports requiring substantial strength and power (e.g., weightlifting, American football). Existing guidelines on best practice management of FeSup to enhance sports performance among high-level female athletes may therefore require refinement, with consideration of new research findings.¹⁷

Current systematic review indicate FeSup may improve the aerobic capacity of IDNA-1 and -2 trained female and male endurance athletes.² However, application of these outcomes are limited as the mechanisms responsible for affecting performance in other physical parameters (e.g., speed, power) in IDNA-1 and -2 or IDA-3 athletes may differ to those affecting endurance performance and aerobic capacity in endurance-trained athletes. The application of these otucomes are complicated when addressing high-level female athletes given the greater rate of iron turnover compared to males, which is reflected by their higher recommended dietary intake (i.e., pre-menopausal females: 18 mg/day, males: 8 mg/day).¹⁸ Furthermore, high-level female athletes are predisposed to larger overall training loads compared to recreationally trained female athletes, thus resulting in a larger daily iron turnover. The application of current guidelines may therefore not be completely appropriate for high-level female athletes.

Sports performance is typically composite of a wide suite of physical measures beyond maximal aerobic capacity and endurance. In the absence of a systematic review examining the effect of iron deficiency on other physical parameters (e.g., strength, power) or performance metrics, the understanding of how to best manage high-level female athletes (e.g., athletes competing in intermittent team) beyond those who compete in principally aerobic-dominant sports (e.g., long-distance running, cycling) is unclear. Therefore, the aim of this review was to characterize the effects of iron deficiency and FeSup on sports performance in high-level female athletes.

2. Methods

2.1. Search strategy

For the purposes of this review, we defined exercise performance as the concurrent interaction of several body systems, including musculoskeletal, cardiovascular, pulmonary, and nervous system, in a non-competitive environment.¹⁹ These interactions contribute to physical (e.g., speed, strength) and physiological (e.g., heart rate, lactate threshold) parameters underpinning exercise performance.¹⁹ However, other endogenous and exogenous factors (technical, mental, and tactical) also interrelate to form the construct of sports performance. The results of sports performance can be reduced to measurable components such as time, speed, and distance, as well as to performance outcomes reflective of success (e.g., competition results, ranking systems).

Secondly, we define high-level female athletes as those described as highly-trained (maximal oxygen uptake (VO_2max) > 45 mL/kg/min, or trained > 5 h/week) collegiate, semi-elite, or elite athletes according to the participant classification framework (Tier 2 and above).²⁰ Preliminary analysis indicated a wide heterogeneity in performance and physiological parameters, complicating the capacity to perform a meta-analysis. Therefore, we elected to conduct a systematic review without meta-analysis.

Our systematic review followed the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) framework in 5 online databases (MEDLINE, SPORTDiscus, Web of Science, Scopus, and CINAHL). Combinations of the following terms were searched in July 2023, including iron, deficien*, supplement*, replet*, athlete*, player*, female*, women*, girl*, perform*, exercise*, sport*, and physical activity.

Search terms were combined using Boolean operators for keywords relating to treatment (deficien* OR supplement* OR replet*), cohort (athlete* OR player*), gender (female* OR women* OR girl*), and sports performance (perform* OR exercise* OR sport* or physical activity). The reference list of identified reviews and all eligible articles were examined individually to identify any additionally relevant articles.

2.2. Eligibility criteria

Studies were included based on the following criteria: (a) participants were females and described as high-level athletes (participant classification framework Tier 2 and above);²⁰ (b) highly-trained athletes with a baseline VO_2max >45 mL/kg/min, or trained > 5 h/week or >20 h/month; (c) the effect of iron deficiency or FeSup was assessed via exercise or sports performance; and (d) participants were classified as ID based on a diagnostic criteria of sFer <40 µg/L. Articles published in languages other than English were excluded, as were editorials, reviews, letters to the editor, abstracts, opinion and commentaries, and duplicate publications. It is important to acknowledge the limitations of utilizing sFer as a sole criterion to categorize iron deficiency given it is an acute phase protein influenced by exercise-induced inflammation. Consequently day-to-day measurements of sFer often exhibit large variation. However, preliminary analysis indicated sFer was the sole homogenous hematological biomarker utilized to categorize the severity of iron deficiency among participating athletes between studies.

2.3. Study selection and data extraction (outcome variables)

Following the initial database searches, independent reviewers (MP and NE) screened the title and abstract of each article using Covidence software (Covidence systematic review software, Veritas Health Innovation, Melbourne, VIC, Australia; available at www.covidence.org). Any discrepancies were resolved through discussion between the 2 independent reviewers (MP and NE), and if a consensus could not be determined, a 3rd independent reviewer (KP) was consulted. Retrieved articles fulfilling the inclusion criteria were accessed in full, and data were extracted using a customized table. For normally distributed data, the mean, SD, and 95% confidence intervals (95%CIs) for all outcome variables were extracted from eligible studies. For non-normally distributed data, the median and the inter-quartile range (IQR) for all outcome variables were extracted.

2.4. Quality of assessment

The methodological quality of included studies was assessed using the Downs and Black Quality Assessment Checklist²¹ and Oxford Level of Evidence.²² The Downs and Black Quality Assessment Checklist was adjusted for the study design, with only 21 of the 27 items deemed appropriate. These items addressed reporting, external validity, internal bias, selection bias, and statistical power. Two reviewers (MP and NE) conducted the assessment independently, with disagreements resolved by a 3rd reviewer (KP). Items were scored as yes (1), no (0), or unable to determine (0), with a final score out of a maximum of 21 obtained by summation. The overall assessment of quality scores were converted to a percentage value and rated as low (0%–49%), moderate (50%–79%), or high (≥80%) quality.

3. Results

3.1. Study characteristics

The flow of records is presented in Fig. 1. The initial search yielded 1221 studies, from which 282 studies were retrieved for full-text review and eligibility assessment. A total of 22 studies met the inclusion criteria. An additional study satisfying the inclusion criteria was identified through screening the reference lists of the included studies, bringing the total to 23. The total number of female athletes was 669 (experimental n = 341; control n = 328; age = 22 ± 6 years; VO_2max = 49.4 ± 6.1 mL/kg/min; training hours per week = 6.4 ± 2.8 h; mean ± SD). Athletes were recruited from 16 sports (62% from aerobic-dominant sports) across 4 performance tiers (49% from Tier 3).²⁰ Table 1 provides a summary of the 7 studies23, 24, 25, 26, 27, 28, 29 examining the effects of iron deficiency on sports performance, and Table 2 details 16 studies30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45 examining the effects of FeSup on sports performance. Detailed results for studies examining the effects of iron deficiency on sports performance are available in Supplementary Material 1, while detailed results for studies investigating the effects of FeSup on sports performance are presented in Supplementary Material 2.

Fig. 1.

PRISMA flow chart presenting the full search strategy for all 5 databases used for the systematic review on the effects of iron deficiency and iron supplementation. PRISMA = preferred reporting items for systematic reviews and meta-analyses.

sFer = serum ferritin; ID = iron deficiency.

Table 1.

Study characteristics of reviewed studies examining the effect of iron deficiency on sports performance in high-level female athletes.

Study	Participant cohort Group: number, age (year)a	Sport Performance level VO2maxa(mL/kg/min); training h/weeka	ID criterion	Trial duration (day) (Iron assessment days)	Main outcome
Auersperger, et al. (2012)23	n = 18 ID: n = 8, 33 ± 6 ctrl: n = 10, 32 ± 5	Running Trained (Tier 2) VO2max: ID = 46 ± 4 ctrl = 49 ± 7	N/Ab	70 (0, 56, 70)	1) ↓ VO2max baseline –6% (p ≥ 0.05) 2) ↓ TT baseline –19% (p ≤ 0.05) 3) ↑ VO2max adaptation +2% and TT adaptation +6%
Auersperger et al. (2013)24	n = 14 ID: n = 7, 35 ± 5 ctrl: n = 7, 31 ± 6	Running Trained (Tier 2) VO2max: ID = 47 ± 5 ctrl = 46 ± 3	sFer <20 µg/L sTfR ≥1.5	63 (0, 56, 63)	1) ↑ VO2max baseline +4% 2) ↓ TT baseline –4% 3) ↑ TT adaptation +5% (p ≤ 0.05) 4) ↑ VO2max adaptation +3% (p ≥ 0.05)
Baranauskas et al. (2020)25	n =14, 26 ± 5	Basketball National (Tier 4) Training h: 6 ± 3	sFer <15 µg/L	0	1) Moderate, positive correlation between transferrin and VO2peak (r = 0.59; p = 0.028) 2) Negative correlation between haematological biomarkers and PWC170, and ferritin and VO2peak (p ≥ 0.05)
Cialdella-Kam et al. (2014)26	n = 18 ID: n = 8, 19 ± 3 ctrl: n = 10, 18 ± 2	“Endurance” athletes Trained (Tier 2) VO2max: ID = 49 ± 6 ctrl = 51 ± 5	N/Ab	0c	1) ↓ VO2max –3% and isokinetic strength –23% to +4% (p ≥ 0.05)
DellaValle et al. (2011)27	n = 149 ID: n = 62 ctrl: n = 87, 20 ± 1	Rowing Collegiate (Tier 3) Training h: 6 ± 2	sFer <20 µg/L	0	1) ↓ 2 km TT –4% (p = 0.004) 2) Negative relationship between sFer < 25 and TT time (B = –17.4; p = 0.01)
Dellavalle et al. (2012)28	n = 48 ID: n = 24 ctrl: n = 24, 20 ± 1	Rowing Collegiate (Tier 3) Training h: 6 ± 4	sFer <20 µg/L	0	1) ↓ 4 km TT –3% (p = 0.03) 2) ↓ TT adaptation –1% and EE adaptation –2% 3) ↓ work rate 0–3.6 km –9% and EE –3% (p ≥ 0.05) 4) ↑ BLa 10-min post 4 km TT + ∼20%
Malczewska-Lenczowska et al. (2010)29	n = 6, 17 ± 0.8	Cross-country skiing Trained/ national (Tier 3) VO2max: 53 ± 2	sFer <20 µg/L sTfR/logFer index >1.8	0	No correlation between sFer and training load score (r = 0.039; p ≥ 0.05)

^aData are shown as Mean ± SD.

^bStudy examined iron status and performance including iron normal athletes. Data were extracted for only the ID athletes.

^cTrial duration was 180 days; however, comparisons between ID and iron sufficient groups were only made when commencing the trial (i.e., 0 day).

Abbreviations: BLa = blood lactate; ctrl = controls; EE = energy efficiency; Fer = ferritin; ID = iron-deficient; N/A= not applicable; PWC170 = peak work capacity at 170 watts; sFer = serum ferritin; sTfR = soluble transferrin receptor; TT = time-trial; VO_2max = maximal oxygen consumption; VO_2peak = peak oxygen consumption.

Table 2.

Study characteristics of reviewed studies examining the effect of FeSup on sports performance in high-level female athletes.

Study	Participant cohort Group: number, age (year)a	Sport Performance level VO2maxa (mL/kg/min); training h/weeka	ID criterion	Trial duration (day) (Iron assessment days) Treatment protocol elemental iron (days, total dose elemental iron)	Main outcome
Axling et al. (2020)30	n = 53 Fe: n = 26, 22 ± 4 ctrl: n = 27, 22 ± 6	“Competitive” athletes Trained (Tier 2) Training: Fe = 8 ± 2 h ctrl = 8 ± 2 h	sFer <20 µg/L Hb >130 g/L CRP <5 mg/L	84 (0, 28, 56, 84) Oral, 4 mg/day (84, 336 mg)	1) ≠ VO2max or time to exhaustion (p ≥ 0.05) 2) ↓ max HR (∼ –0.5 bpm) and max BLa (∼ –0.5 mmol.L) (p ≥ 0.05)
Bell et al. (1994)31	n = 15 Fe: n = 5 ctrl: n = 10, 19	Basketball Collegiate (Tier 3) VO2max: Fe = 51 ± 10 ctrl = 55 ± 5	sFer <15 µg/L	∼197 (0, ∼99, ∼197) Oral, 100 mg/day (42, 4200 mg)	1) ↑ VO2max +9% (p ≥ 0.05) 2) ↑ peak power +9% (p ≥ 0.05) 3) ↑ avg power +7% (p ≥ 0.05) 4) ↔ between groups (p ≥ 0.05)
Blee et al. (1999)32	n = 29 Fe: n = 15, 19 ± 3 ctrl: n = 14, 18 ± 2	Netball National (Tier 3) VO2max: Fe = 47 ± 2 ctrl = 48 ± 2	sFer <40 µg/L Hb >125 g/L	18–20 (0, 13–15, 18–20) Intramuscular, 100 mg bi-daily (10,500 mg)	1) ≠ VO2max or max power (p ≥0.05) 2) ↓ average power –3% (p ≥ 0.05) 3) ↔ between groups (p ≥ 0.05)
Brownlie IV et al. (2002)33	n = 41 Fe: n = 22 ctrl: n = 19, 18–33b	Physically active Trained Tier 2) VO2max: Fe = 49 ± 2 ctrl = 55 ± 2	sFer <16 µg/L Hb >120 g/L	36 (0, 18, 36) Oral 16 mg/day (36,576 mg/day)	1) ↑ VO2max +15% (p ≤ 0.05) 2) ↔ between groups (p ≥ 0.05)
DellaValle et al. (2014)34	n = 31 Fe: n = 15, 20 ± 1 ctrl: n = 16, 20 ± 1	Rowing Collegiate (Tier 3) Training: 6 ± 4 h	sFer <20 µg/L	42 (0, 21, 42) Oral, 16 mg/day (42,672 mg)	1) ↑ 4 km times +2% (p ≥ 0.05) 2) ↑ max work rate +11% (p = 0.00) 3) ↑ EE +2% (p = 0.03) 4) Fe slower BLa rise <2 km (+11%; p = 0.001) 5) Fe faster BLa recovery 5 min post TT (+8%; p = 0.001)
Fogelholm et al. (1992)35	n = 31 Fe: n = 14, 24 (21–26) ctrl: n = 17, 21 (20–24)c	Running + team sports Trained (Tier 2) Training: Fe = 8 (7–10) h ctrl = 9 (7–11) hc	sFer <25 µg/L Hb >120 g/L	56 (0, 56) Oral, 16 mg/day (56,896 mg)	1) ↑ VO2max +1% and max BLa +81% (p ≥0.05) 2) ≠ max HR (p ≥ 0.05)
Friedmann et al. (2001)36	n = 23 Fe: n = 11, 16 ± 2 ctrl: n = 12, 16 ± 2	“Endurance” athletes National (Tier 3) VO2max: Fe = 46 ± 7 ctrl = 43 ± 5	sFer <20 µg/L	84 (0, 84) Oral, 100 mg/d ay (84, 8400 mg)	1) ≠ VO2max, max HR, max BLa, or LT (p ≥ 0.05) 2) ↔ between groups (p ≥ 0.05)
Klingshirn et al. (1992)37	n = 18 Fe: n = 9, 29 ± 6 ctrl: n = 9, 28 ± 4	Running Trained (Tier 2) VO2max: Fe = 50 ± 5 ctrl = 52 ± 4	sFer <20 µg/L	56 (0, 56) Oral, 100 mg/day (56, 5600 mg)	1) ↓ VO2max +2% 2) ↑ time to exhaustion +20% and max BLa +30% 3) ↔ between groups (p ≥ 0.05)
Newhouse et al. (1989)38	n = 40 Fe: n = 20 ctrl: n = 20, 18–40b	Running Trained (Tier 2) VO2max: Fe = 51 ± 6 ctrl = 51 ± 5	sFer <20 µg/L Hb >120 g/L	63 (0, 63) Oral, 100 mg/day (56, 5600 mg)	1) ↑ VO2max +3% and LT +1% (p ≥0.05) 2) ↓ alactic power –5%, (p ≥ 0.05) 3) ≠ lactacid power or max treadmill velocity (p ≥ 0.05)
Peeling et al. (2007)45	n = 16 Fe: n = 8, 25 ± 10 ctrl: n = 8, 33 ± 7	“Endurance” athletes Trained (Tier 2) VO2max: Fe = 47 ± 3 ctrl = 52 ± 2	sFer <35 µg/L Hb >115 g/L	28 (0, 20, 28) Intramuscular, 100 mg bi-daily (8–10, 500 mg)	1) ↑ time to exhaustion +18% (p ≤ 0.05) 2) ↑ VO2max +3% (p ≥ 0.05) 3) ↓ BLa 1 min post +18% and 5 min post +13% (p ≤ 0.05) 4) ↔ between groups (p ≥ 0.05)
Schoene et al. (1983)39	n = 15 Fe: n = 9, 20 ± 1 ctrl: n = 6, 22 ± 7	Variety Collegiate and trained (Tiers 2 and 3) VO2max: Fe = 45 ± 8 ctrl = 48 ± 12	sFer <20 µg/L Hb >11.5 g/L	28 (0, 14, 28) Oral, 100 mg/day (14, 1400 mg)	1) ↑ VO2max and workload +1% (p ≥0.05) 2) ↓ max Bla +23% (p ≤ 0.04)
Shaw et al. (2023)40	n = 28 LPAP: n = 10, 35 ± 8.6 pea: n = 8, 35 ± 13 ctrl: n = 10, 34 ± 8.6	Running Trained VO2max: LPAP = 53 ± 8 pea = 54 ± 9 ctrl = 50 ± 8	N/Ad	48 (0, 48) Diet, 6 mg/day (48, 298 mg)	1) ↔ VO2max (–14% to –6%; p = 0.64) or 5 km running time trial performance (0%–1%; p = 0.55) within groups or between groups
Sitkowski et al. (2019)41	n = 7 Fe: n = 3 ctrl: n = 4, 21 ± 3	Cycling National (Tiers 4 and 5) VO2max: Fe = 58 ± 0 ctrl = 56 ± 2	sFer <35 µg/L	39–45 (0, 39–45) Oral, 6 mg/day (21, 118 mg)	1) ↑ VO2max and PAT4 +3%
Tsalis et al. (2004)42	n = 13 Fe: n = 4, 15 ± 1 Diet: n = 5, 15 ± 1 ctrl: n = 4, 15 ± 1	Swimming National (Tier 3) Training:e >5 h/week	N/Af	168 (0, 84, 140, 168) Oral, 47 mg/day (168, 7896 mg)	1) ↑ 25 m (+3%), 200 m (+8%), and 2000 m (+2%) swimming velocity and swimming velocity at LT (+10%)
Wachsmuth et al. (2015)43	n = 30 severe ID: n = 8, 24 ± 4 mild ID: n = 14, 25 ± 5 ctrl: n = 8, 28 ± 10	“Recreational” athletes Trained (Tier 2) VO2max: SID = 45 ± 6 MID = 47 ± 7 ctrl = 47 ± 8	sFer <25 µg/L	98–210 (0, 21, 35, 56, 70–126, 98–154, 154–210)g Oral, 100 mg/day (70–126, 7000–12,600 mg)	1) ↑ VO2max +6% (p ≥0.05) 2) Positive correlation beween ∆ Hbmass and ∆ VO2max (y = 2.3 x –4.3; r = 0.65; p ≤ 0.01)
Yoshida et al. (1990)44	n = 12 Fe: n = 6, 20 ± 1 ctrl: n = 6, 20 ± 1	Running Trained (Tier 2) VO2max: Fe = 54 ± 4 Ctrl = 53 ± 5	sFer <20 µg/L	56 (0, 56) Oral, 60 mg/day (56, 3360 mg)	1) ↑ 3000m running performance +4%, LT +7%, OBLA running velocity +4%, and (p ≤ 0.05) 2) ↑ VO2max +1% (p ≥ 0.05)

^aData presented as Mean ± SD.

^bData presented as a range.

^cData presented as median (inter-quartile range).

^dNo criterion applied within the study to categorize iron deficiency. Mean sFer values(μg/L) were LPAP = 33.4 ± 19.2, pea = 33.4 ± 22.6, and ctrl = 31.3 ± 12.2.

^eSwam 6 km/day during the 1st phase, 5 km/day during the 2nd phase, 3 km/day during taper in addition to 3×45 min resistance training session per week during each phase.

^fStudy examined iron status and performance including iron normal athletes. Data were extracted for only the ID athletes.

^gAthlete supplemented an additional 4–8 weeks if they remained iron deficient.

≠ no change; ↔ no difference; ↑ increase; ↓ decrease.

Abbreviations: BLa = blood lactate; CRP = C-reactive protein; ctrl = controls; EE = energy efficiency; Fe = iron treated; Hb = hemoglobin; HR = heart rate; LPAP = low phytic acid pea power; LT = lactate threshold; MID = mild iron deficiency; N/A = not applicable; OBLA = onset of blood lactate accumulation; PAT4 = power at 4 mmol/L⁻¹ lactate; pea = normal pea powder; sFer = serum ferritin; SID = severe iron deficiency; TT = time-trial; VO_2max = maximal oxygen consumption.

Seven studies23, 24, 25, 26, 27, 28, 29 examined the effect of iron deficiency on sports performance in female athletes (Table 1). A total of 267 athletes (age = 21 ± 5 years; VO_2max = 48.1 ± 4.8 mL/kg/min; training hours per week = 6.2 ± 2.7 h, mean ± SD) were recruited, with 95% competing in aerobic-dominant sports. Athletes were representative of 3 performance tiers (with 76% categorized as highly trained and national level athletes Tier 3). The majority of the studies (n = 5) utilized a sFer criterion of < 20 µg/L. All comparisons for each study were made between ID and iron sufficient (IS) athletes based on the diagnostic criteria of sFer < 40 µg/L to categorize iron deficiency.

Sixteen studies30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45 examined the effect of FeSup on sports performance among ID female athletes (Table 2). A total of 402 athletes (age = 23 ± 7 years; VO_2max = 49.7 ± 6.3 mL/kg/min; training hours per week = 7.0 ± 3.1 h) were recruited, with 50% competing in aerobic-dominant sports. Athletes were representative of 4 performance tiers (with 67% categorized as trained and development-level athletes (Tier 2)). The majority of the studies (n = 9) utilized an sFer criterion of < 20 µg/L. Total elemental FeSup doses ranged from 336 mg to 8400 mg, with daily doses ranging from 4 mg to 100 mg per day or bi-daily. Both the FeSup and placebo comparison groups in each study were ID based on the diagnostic criteria of sFer < 40 µg/L prior to any supplementation. Four studies reported on negative symptoms experienced from FeSup.^34,36,37,40 Only 1 athlete discontinued participation due to gastic discomfort.³⁷ There was a greater prevalence (∼40%) of negative symptoms from dietary intervention, although the prevalence declined throughout the study with no differences between comparison groups.⁴⁰

Dietary, menstruation, and training data were reported in 48%,^25,26,28,32, 33, 34, 35^,37,40,42,45 35%,26, 27, 28^{,33,34,38,42,43,45} and 78%23, 24, 25, 26, 27, 28, 29, 30^{,33,35,37,38,}40, 41, 42, 43, 44, 45 of all studies, respectively. No study accounting for diet or menstruation observed an effect of either variable on performance. While reported to have no effect on outcome variables, only duration/mileage and/or training frequency in 5 studies^{26,30,35,37,45} accounted for training data.

Without more training detail (e.g., intensity), it is difficult to interpret the effect of varied training programs on physical and physiological parameters. Four studies^31,32,34,36 not accounting for training data had athletes completing the same or similar unlogged training sessions.

3.2. Quality of assessment

The methodological quality of included studies is detailed in Supplementary Materials 3 and 4. The overall quality of assessment score using the modified Downs and Black Quality Assessment Checklist (21 items) was 77% ± 13% ranging from 57% to 100%. One study³⁴ achieved a total score of 100%, with 10 studies^25,27,28,32, 33, 34^,40, 41, 42^,45 achieving a high-quality score (≥80%) and the remaining 13 studies^23,24,26,29, 30, 31^,35, 36, 37, 38, 39^,43,44 receiving a moderate quality score (50%–79%).

3.3. Iron deficiency and physical parameters

The effect of iron deficiency on maximal aerobic capacity was variable, ranging from –6% to +4%.^23,24,26 Peak oxygen uptake (VO_2peak) was assessed using a graded exercise test in 1 study.²⁵ There was a weak negative correlation between sFer and VO_2peak (r = –0.39) and a moderate positive correlation between transferrin and VO_2peak (r = 0.59).²⁵ IS trained athletes completed time-trials assessing endurance performance 1%–19% faster than ID athletes.^23,24,27,28 Furthermore, ID athletes produced 2% less energy as measured via indirect calorimetry during a 4 km rowing time-trial.²⁸

Only 1 study²⁶ explored the effects of iron deficiency on power measured as isokinetic strength However, another study that examined the effects of FeSup on sports performance measured anaerobic power (10 s maximal sprint and 5 × 6 s repeated sprints) pre-test, prior to any FeSup.³¹ Isokinetic strength measured across 3 velocities was impaired by up to –23% in 10 out of 12 assessments in ID athletes.²⁶ Likewise, peak and mean power output were 6%–10% lower in ID athletes.³¹

Two studies^28,29 investigated whether training loads are reduced among ID athletes, while another 2 examined whether iron deficiency impaired adaptation to training.^23,24 There was no significant correlation between sFer and training load score,²⁹ although collegiate rowers reported training for 10 min less per day.²⁸ Maximal aerobic capacity showed variable changes (+2% to 3%), while endurance performance improved in both ID (+5% to 6%) and IS (+6%) athletes following 8-week endurance-training programs.^23,24

3.4. FeSup and physical parameters

The effect of FeSup on maximal aerobic capacity varied from –3% to +15%, with no significant differences in performance between athletes receiving FeSup or placebo. Iron-supplemented athletes completed endurance protocols (i.e., time-trial) either slower or simultaneously with placebo-treated athletes when FeSup protocols were <100 mg/day.^30,34,40 Time-to-exhaustion improved by ∼20% when FeSup protocols involved 100 mg of elemental iron either per day, following oral supplementation across 56 days,³⁷ or bi-daily via parenteral administration over 8–10 days.⁴⁵

Assessed via 10–15 s maximal efforts on a cycle ergometer, peak and mean power output improved by 6%–9% following FeSup of 100 mg/day of elemental iron for 6 months, although these differences were not different from placebo-treated athletes.³¹ There was a 0%–5% reduction in peak power outputs averaged across 5-s, 10-s, and 30-s efforts on a cycle ergometer.^31,32,38 There were also similar reductions in mean power output, measured across 5×6 s repeated sprints on a cycle ergometer, as well as vertical jump following oral supplementation of 100 mg/day of elemental iron over 63 days or parenteral administration of 100 mg of elemental iron delivered bi-daily over 8–10 days.³²

3.5. FeSup and physiological parameters

There was no significant effect of FeSup on peak heart rate, mean velocity at lactate threshold, or maximal blood lactate (BLa) concentration (1%–3%), nor were differences found between iron- and placebo-treated athletes during assessment of maximal aerobic capacity.^{33,35,36,39,40,45} Maximal BLa post-supplementation varied by –23% to +81% following maximal exhaustion.^35,39 Individual data were not presented for 2 studies^30,36 utilizing graded exercise tests, though there were no significant intragroup or intergroup differences in maximal BLa post-supplementation

There were substantial differences in mean velocities at lactate threshold and measures of BLa (maximal, during performance, and during recovery) when assessing endurance performance.^{34,37,42,44,45} Running and swimming velocities at lactate threshold and onset of BLa accumulation (OBLA), improved by 4%–10% after 16 mg/day–60 mg/day of elemental iron over 42–168 days^34,42,44 compared to baseline values. BLa concentrations improved by 7%–30% following FeSup of 16 mg/day–100 mg/day of elemental iron over 42–56 days.^34,37 Energy efficiency, maximal work rates, and maximal velocities improved by 2%–8% following 47 mg/day–60 mg/day over 56–168 days during endurance protocols but not during assessment of maximal aerobic capacity.^34,42,44

4. Discussion

The impact of iron deficiency in high-level female athletes appears largely dependent on the severity of iron deficiency, particularly regarding endurance performance and maximal work rates.²⁷ Furthermore, ID athletes require more energy to complete the same endurance task. IDNA-1 and -2 athletes do not typically exhibit compromised Hb concentration, thus performance decrements experienced with respect to maximal aerobic capacity, strength, and anaerobic power may become more pronounced in IDA-3 athletes in whom Hb concentrations are reduced below the clinical threshold (≤119 g/L).

4.1. Iron deficiency and physical parameters

The effects of iron deficiency on maximal aerobic capacity and endurance performance is influenced by factors including the choice of testing protocol (laboratory or field), athlete's performance level, and the diversity of athletes from multiple sports. Iron deficiency consistently impairs endurance performance (e.g., time-trial, time-to-exhaustion); however, the effects of IDNA-1 and -2 on maximal aerobic capacity are inconsistent. Many studies recruited IDNA-1 and -2 athletes, thus complicating understanding as marked differences between IDNA-1 and -2 athletes and IS athletes appear unlikely. For this reason, only athletes with Hb concentrations ≤119 g/L typically experience impaired oxygen transportation. This assertion is supported by Baranauskas, et al. ²⁵ who observed no significant correlation between sFer and peak oxygen uptake measured in a graded exercise test, indicating that reduced Hb below the criterion of ≤119g/L for IDA-3 may be the limiting factor in such protocols. Subsequently, while IDNA-1 and -2 athletes may exhibit compromised energy production, possibly due to a reduction in tissue oxidative capacity, their maximal aerobic capacity may not be substantially affected. This effect could be attributed to the shorter duration of demanding workloads above those that can be sustained aerobically during a graded exercise test, which typically involves stages lasting 1–2 min^23,24,26 compared to endurance protocols ranging from ∼8–18 min.^23,24,27,28

In protocols with longer durations, IDNA-1 and -2 athletes may be unable to sustain the same workloads aerobically as IS athletes, consequent to impaired tissue oxidative capacity.²⁸ Endurance performance was compromised by 3%–19% among ID athletes compared to their IS counterparts.^23,24,27,28 However, only 1 study²⁸ examined proxy measures related to tissue oxidative capacity (i.e., BLa, energy efficiency), thus more research is warranted to confirm the notion that a reduction in tissue oxidative capacity is responsible for compromised endurance performance among IDNA-1 and -2 athletes. A more direct measure of tissue oxidative capacity (e.g., iron-dependent oxidative enzymes in muscle) would be beneficial. Nevertheless, the 3%–19% decrements in endurance performance highlight the extent to which sports performance may be compromised for ID athletes competing in a range of endurance sports (e.g., 10,000 m track; 1500 m swim).

The athlete's performance level (Tiers 1–5) also appears to influence the effect of iron deficiency on maximal aerobic capacity and endurance performance. Higher-level athletes (collegiate to national; Tiers 3–5) may be more sensitive to performance deficits compared with lower-level athletes (trained and development-level; Tier 2). While no substantial differences in maximal aerobic capacity were observed between ID and IS trained athletes and development-level athletes (Tier 2),^23,24,26 collegiate ID athletes (Tier 3) displayed inferior maximal aerobic capacity compared to their IS counterparts.³¹ This outcome suggest that higher-level athletes (Tiers 3–5) may have fewer lifestyle (e.g., work) and performance (e.g., training load) factors that fluctuate greatly, which could account for differences in performance compared to lower-level athletes. It is important to note that all athletes included in these studies can only be presumed to be IDNA-1 and -2 as Hb concentrations were not always measured when categorizing iron deficiency.^23,24,26 It would have been more appropriate to assess the athlete's endurance, given Hb concentrations may only affect maximal aerobic capacity in athletes with Hb concentrations ≤119 g/L.

The effect of iron deficiency on strength and power in high-level female athletes may be trivial, but a comprehensive understanding is constrained by the few studies investigating this area. Isokinetic strength and anaerobic power was inferior by up to –23% in ID athletes, but neither of these outcomes were considered significant.^26,31 While the limited sample size in both studies (ID: n = 8²⁶ and n = 5³¹) likely influenced the interpretation of results, it appears an athlete's performance level does not exacerbate decrements in performance caused by ID but other mechanisms affecting performance. The attenuated strength and power observed in ID athletes may depend on Hb concentration, thereby only consistently affecting IDA-3 athletes. Although strength and power do not directly rely on iron indices during single sets of resistance training or short bursts of maximal power, Hb is critical for tissue oxygenation and subsequent recovery. Reduced tissue oxygenation in athletes with low Hb concentrations may limit strength and power output due to reduced recovery between efforts, yielding inferior adaptation and attenuated performance. This is particularly relevant for IDA-3 athletes with compromised Hb concentrations. Conducting more studies, especially with a larger sample size, can provide a better understanding of the effects of iron deficiency on strength and power in high-level female athletes. This research will inform ID athletes in sports characterized by strength and power (e.g., gymnastics, powerlifting) of performance deficits they may be predisposed to.

The effect of iron deficiency on training loads and longer-term adaptation to training is difficult to interpret. The homogeneity in iron status of the athletes (sFer < 20 µg/L) makes it challenging to analyze associations between sFer and training load scores.²⁹ The lack of diversity in athletes with varying sFer stores may account for lack of associations between sFer and training load score. However, ID athletes have reported training less per training session compared to their IS counterparts. The reduced training time among ID athletes may contribute to their lower VO_2peak compared to IS athletes, although longitudinal training loads were associated to a single measure of iron status.²⁸ However, concerning adaptation to training, IDNA-1 and -2 athletes show little impairment. Trained ID runners improved both maximal aerobic capacity (2%–3%) and endurance performance (5%–6%) following an 8-week training intervention.^23,24 Although only the improvements in endurance performance reached statistical significance, the limited number of ID athletes included in the study²⁴ (n = 7) may have hindered the detection of small but meaningful changes in maximal aerobic capacity. Nevertheless, ID runners recorded 2400 m time-trial times that were approximately 36 s slower than IS runners. It appears that sports performance is likely inferior among ID athletes, regardless of their ability to improve following training interventions. Future studies should include IS athletes to provide a better understanding of the relationships between sFer values and training load scores.

While ID athletes likely have compromised endurance compared to their IS counterparts, evidence on maximal aerobic capacity remains equivocal, and data on strength, anaerobic power, and training loads is in its infancy. One limitation of studies investigating iron deficiency without FeSup is that they omit the potential benefits of supplementation. While it may appear that iron deficiency does not directly affect performance, it is important to understand whether ID athletes would benefit from FeSup. Further research examining the impact of iron deficiency on various performance measures would help clarify the effects on sports performance and guide appropriate interventions for athletes.

4.2. FeSup and physical parameters

The effectiveness of FeSup on endurance performance in high-level female athletes appears to only be beneficial when dosage protocols exceed 100 mg of elemental iron per day or bi-daily, either orally (up to 56 days) or through parenteral administration (over 8–10 days).^37,45 Lower dosages of FeSup may not have any practically worthwhile effect on performance.^30,34 For example, while iron-treated collegiate rowers recorded 4 km time-trial times 30 s slower following FeSup of 16 mg/day of elemental iron for 42 days, consumption compliance was only ∼60%.³⁴ The recommended dose proposed to benefit ID athletes is generally >100 mg of ferrous compounds⁴⁶ containing 20 mg of elemental iron. The recommended dietary intake for iron in pre-menopausal female athletes is 18 mg/day of elemental iron, with FeSup compliance among the collegiate rowers equating to 15 mg/day of elemental iron compared to the initially prescribed 20 mg/day. The associations between FeSup compliance and the effects on 4 km rowing time-trial performance would therefore have been of greater interest in determining the benefits of FeSup on endurance performance. This sentiment is echoed by Axling, et al. ³⁰ who found that the total daily dose equated to 5-fold lower (∼4 mg elemental iron) than the recommended dose proposed to benefit ID.⁴⁶

Insufficient iron stores can negatively impact oxygen transportation along complex I, III, and IV in the electron transport chain, as succinate dehydrogenase, ubiquinone, and cytochrome C each contain iron sulfur clusters.⁹ The minimal FeSup protocol (e.g., 4 mg/day of elemental iron) in ID athletes may have been too low to enhance the effectiveness of these components, thereby limiting ATP production. The modest effects of these FeSup protocols is reflected in the absence of improvements in time-to-exhaustion³⁰ and 4-km time-trial times³⁴ following 36–98 days of supplementation. However, it is worth noting that the primary focus of the Axling, et al. ³⁰ study was the effect of Lactobacillus plantarum 299v on performance, with the experimental group and control group both receiving ∼4 mg/day of elemental iron. Therefore, any difference in time-to-exhaustion between groups is difficult to discern. Sports performance reliant on endurance (football, triathlon) may be enhanced among high-level ID female athletes with 100 mg of elemental iron delivered daily or bi-daily via oral supplementation (up to 56 days) or parenteral administration (over 8–10 days). However, further research is required to confirm whether proposed dosages to enhance performance (i.e., 20 mg/day of elemental iron) are sufficient to enhance endurance.

The effectiveness of FeSup for enhancing maximal aerobic capacity appears to coincide with the severity of iron deficiency. There appears to be little effect of FeSup in athletes with higher sFer values (e.g., sFer >25 µg/L).^30,32,35, 36, 37, 38, 39, 40, 41^,43, 44, 45 Conversely, maximal aerobic capacity improved by 6%–15% following 16–100 mg/day for 36–126 days in studies utilizing a sFer criterion of <16 µg/L.^31,33,43 These findings challenge the proposition that maximal aerobic capacity is only compromised in IDA-3 athletes, rather supporting the notion that performance decrements coincide with the severity of iron deficiency. Therefore, IDNA-2 athletes with low sFer (<15 µg/L) and normal Hb concentrations (≥120 g/L), may still exhibit a compromised maximal aerobic capacity given the tissue oxidative capacity is further diminished with lower iron stores. However, ID athletes competing in sports demanding exertion near maximal aerobic capacity with sub-optimal sFer concentrations (<16 µg/L) should seek advice from a qualified practitioner.

Hb concentration or derivatives (e.g., Hb mass) were only measured in 3 studies^39,43,45 examining the effect of FeSup on maximal aerobic capacity. However, in 2 of these studies,^39,45 athletes were classified as IDNA-2 (sFer < 20 µg/L; Hb ≥ 120g/L). Consequently, no marked differences in baseline maximal aerobic capacity were evident as no athletes had compromised Hb concentrations. Nonetheless, a 6% improvement in maximal aerobic capacity was observed in trained athletes with severe iron deficiency (sFer < 12 µg/L) following 100 mg/day of elemental iron for a minimum of 70 days.⁴³ Furthermore, a large correlation was evident between Hb mass and the increase in maximal aerobic capacity; though, repeated measures between participants may have introduced bias in the estimates of Pearson's correlation.⁴³ Nevertheless, this result alludes to the effect of a reduction in oxygen transportation to the skeletal muscles and ultimately maximal aerobic capacity. It is crucial to consider the Hb levels of the athletes, particularly those in an anemic state (Hb ≤ 119 g/L), when assessing their maximal aerobic capacity. Appropriate protocol selection (i.e., time-trial, time-to-exhaustion) is important to differentiate performance changes among ID athletes with higher sFer stores when Hb concentration is not the limiting factor.

Interpretation of the effect of FeSup on maximal aerobic capacity is further complicated by differences in athlete's performance levels.³⁹ Athletes were recruited from various intercollegiate (Tier 3) sports teams (e.g., coxswain, golf, tennis), local cycling, and track clubs (Tier 2; highly-trained).³⁹ The variance in performance levels is reflected in the range of maximal aerobic capacity values observed, with the highest VO_2max (63.2 mL/kg/min), nearly double that of the lowest (34.6 mL/kg/min).³⁹ The heterogeneity of maximal aerobic capacity is further compounded by the inclusion of athletes competing in sports not typically characterized by high aerobic capacity (e.g., golf, coxswain). It would be beneficial to compare a homogeneous sample of athletes focused on endurance-based disciplines, such as collegiate rowers. Alternatively, statistically adjusting the model by including baseline VO_2max values as a covariate would isolate the effects of FeSup on aerobic capacity. Attention to these points will facilitate critical insights on IDA-3 athletes in sports demanding exertion near maximal aerobic capacity.

Power output, including explosive efforts (vertical jump test) and anaerobic power in short-duration efforts (<10 s and <30 s), may only be negatively impacted in IDA-3 athletes. In such cases, reduced tissue oxygenation may hinder adaptation to training.^31,32,38 Studies examining the effects of FeSup on power output have generally recruited athletes with Hb concentrations exceeding those indicative of an anemic state (Hb ≥ 120 g/L).^31,32,38 Consequently, the outcomes have been mixed, ranging from decrements of around –5% to improvements of approximately +9% in power measures among iron-supplemented athletes.^31,32,38 Furthermore, it is challenging to isolate the effects of various individual training protocols on performance improvements within each study. It is reasonable to expect only a trivial change in strength and power performance following FeSup in the absence of a resistance training program specifically aimed at enhancing power output. Further research is warranted to assess how FeSup affects a range of power assessments among high-level ID female athletes and to clarify the mechanisms by which performance may be impeded.

4.3. FeSup and physiological parameters

Energy efficiency, maximal work rates, and maximal velocities sustainable during high-intensity aerobic efforts may benefit from FeSup.^34,44 With a reduction in the efficacy of succinate dehydrogenase, coenzyme Q, and cytochrome C, a greater reliance is placed upon glycolysis for producing energy. ID rowers who received FeSup for 42 days improved their energy efficiency by 2%. Comparatively, the placebo group decreased their energy efficiency by 2%.³⁴ Moreover, a reliance upon glycolysis appears to diminish the work rates that can be sustained when the effectiveness of generating ATP aerobically is impeded. These mechanisms may explain why maximal velocities are consistently reduced during aerobic protocols^34,42,44 but not during anaerobic protocols.^38,42 However, FeSup can improve energy efficiency,³⁴ maximal work rates,³⁴ and maximal velocities^42,44 when delivered in daily doses of 16–60 mg of elemental iron (42–168 days). Athletes competing in sports characterized by repeated, high-intensity efforts with short intermittent periods of recovery (e.g., tennis, netball) may therefore be capable of performing subsequent efforts at greater intensities given the production of ATP aerobically, which otherwise is limited without the aid of FeSup.

The effect of FeSup on mean velocities at lactate threshold during sports performance (e.g., 3000 m steeplechase) may be minimal. Lactate threshold should not be affected in IS athletes with a normal Hb concentration. Comparatively, when the electron transport chain is impaired, and a greater reliance on energy production is made on anaerobic pathways, the point at which lactate accumulation exceeds removal should occur at a lower workload. The likelihood of observing an effect of FeSup on mean velocities at lactate threshold may be influenced by the choice of aerobic assessment protocol. Several studies reported improvement in maximal aerobic capacity after long-term FeSup in endurance athletes.^36,38,41 However, an increase in 3000 m running velocity at lactate threshold (+6%) and OBLA (+4%) was observed,⁴⁴ as well as improved swimming velocities < 2000 m at OBLA (+10%).⁴²

Investigators need to account for longer term adaptations to training. In the swimming study, each comparison group improved swimming velocities < 2000 m at the lactate thresholds, implying the results may be attributed to training effects rather than FeSup alone.⁴² Given the small sample sizes in the study,⁴² it is difficult to determine the exact cause of the improvements in swimming velocities at the lactate threshold. However, Yoshida, et al. ⁴⁴ observed significant improvements in 3000 m running velocity at lactate threshold, which provides promising results. Consistent with the FeSup protocols enhancing maximal velocities, sports performance at the lactate threshold benefitted from lower iron doses over longer durations (47–60 mg/day of elemental iron for a minimum of 56 days).^42,44 It appears the work intensities that an athlete can sustain aerobically may be heightened with FeSup.

The testing protocol used in studies to evaluate aerobic performance may explain why iron supplementation does not seem to affect measures of BLa. There appears to be little effect of FeSup on maximal BLa when measured during a graded exercise test.^30,35, 36, 37 However, contrasting results have been observed during endurance tests, where maximal BLa, BLa during time-trial, and BLa recovery are 3%–23% higher.^34,37,45 Only a single study³⁹ measuring maximal BLa from a graded exercise test yielded lower maximal lactate levels following FeSup. Conversely, several studies have reported lower maximal BLa concentrations, lower BLa during time-trial performance, and faster BLa recovery throughout endurance testing when athletes were supplemented with the equivalent of 16 mg/day–100 mg/day of elemental iron for 14–56 days via oral supplementation^34,37,39 or 100 mg delivered bi-daily via parenteral administration over 8–10 days.⁴⁵

The selection of appropriate aerobic tests for ID athletes is crucial, particularly when oxygen delivery is not the limiting mechanism. It is expected that IDNA-1 and -2 athletes would exhibit higher BLa concentrations during endurance protocols compared to IS athletes. This effect relates to the increased reliance on glycolysis to generate energy due to reduced efficacy in energy production through cellular respiration.³⁴ Subsequently, the clearance of lactate among IDNA-1 and -2 athletes may be attenuated. It appears measures of BLa may be improved during endurance sports via lower dosages (e.g., 16 mg/days of elemental iron) over longer durations (e.g., 42 days) or higher dosages (e.g., 100 mg/day of elemental iron) over shorter durations (e.g., 14 days). Athletes competing in sports eliciting high BLa concentrations (e.g., handball, rowing) may therefore benefit from FeSup shifting the BLa curve downwards and rightwards to allow athletes to complete a task aerobically that otherwise, without supplementation, may depend on glycolysis.

4.4. Limitations

There is potential for language bias as only peer-reviewed articles written in English were considered for inclusion. This may have excluded relevant studies published in other languages. Secondly, marked differences in methodological design (e.g., outcome measures, dose protocol) were evident between studies, complicating the interpretation and application of results. Differences in the route of administration of the supplement and the many forms of oral supplementation (e.g., ferrous sulfate, ferrous fumarate) further complicate comparisons; therefore, only estimates of elemental iron can be provided. Finally, given high-level (Tiers 2–5) female athletes differ from the general population and male counterparts, these outcomes are only specific to high-level female athletes. Further research with standardized methodologies and larger sample sizes are needed to provide more conclusive evidence on the impact of iron deficiency and FeSup on sports performance, and to meet the needs of different athlete cohorts and sports.

4.5. Practical implications

Endurance performance may be impeded in ID high-level female athletes. However, performance may be improved with the equivalent of 100 mg of elemental iron per day or bi-daily, either orally for up to 56 days or through parenteral administration over 8–10 days. These findings are consistent with those previously established by Sim, et al.¹⁷ who generally advocate for FeSup of 100 mg of elemental iron per day or bi-daily irrespecitive of the physical or physiological parameter of interest. Contrasting these recommendations, ID high-level female athletes may benefit from consuming 16–60 mg of elemental iron delivered daily for a duration of 42–56 days to enhance energy efficiency and maximal work rates. While IDA-3 athletes and IDNA-2 athletes with low sFer levels (<15 µg/L) may experience compromised maximal aerobic capacity, only IDA-3 high-level female athletes may experience reductions in strength and power. The exact mechanism by which strength and power are hindered is not fully understood, but reductions in tissue oxygenation between efforts could potentially inhibit subsequent strength performance. Nevertheless, high-level female athletes with iron deficiency are encouraged to consult a sports medicine practitioner or sports dietitian to limit compromises in training and competitions while also ensuring FeSup protocols adhere with anti-doping agencies.

5. Conclusion

Endurance performance appears to be negatively affected among ID high-level female athletes but can be improved following FeSup. It is difficult to characterize the effects of iron deficiency and FeSup on a full suite of physical and physiological parameters beyond endurance performance. Data indicate that maximal work rate and energy efficiency can be improved in high-level ID female athletes. This advice is relevant for athletes competing in sports typified by long-sustained, high-intensity efforts as well as those characterized by repeated sprint efforts. Maximal aerobic capacity does not appear to be compromised in IDNA-1 and -2 female athletes with higher sFer stores (>16 µg/L) as their performance is not hindered by low Hb levels or a substantially diminished tissue oxidative capacity. Iron deficiency does not seem to affect strength and power in athletes with IDNA-1 and -2. However, further research is needed to understand how IDA-3, which is associated with compromised Hb concentrations, impacts athletic performance.

Authors’ contributions

MP and KP designed the study, performed the database search, screening process, interpretation of results, drafted and contributed to the final manuscript; DBP designed the study, contributed to the interpretation of the results, drafted and contributed to the final manuscript; NE designed the study, performed the screening process and interpretation of the results, drafted and contributed to the final manuscript. All authors have read and approved the final version of the manuscript, and agree with the order of presentation of the authors.

Competing interests

The authors declare that they have no competing interests.