Iron – Metabolism, Deficiency, and Exercise Effects

Table of Contents

1. Trace Elements – Definitions and Classification
2. Iron as an Essential Trace Element
3. Iron Metabolism: Absorption and Distribution
4. Iron-Containing Proteins
5. Regulation of Iron Homeostasis: Hepcidin
6. Interactions with Other Trace Elements
7. Iron Deficiency in Sports
8. Diagnostic Pathway: Stepwise Laboratory Interpretation
9. Exercise Effects on Iron Status
10. Practical Implications
11. References
12. One-Minute-Paper Topics

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1 Trace Elements – Definitions and Classification

Trace element (Spurenelement): minerals required in amounts between 1 and 100 mg/day or that make up less than 0.01 % of total body weight (Mehri, Int J Prev Med, 2020).

Essential trace element: cannot be synthesised by the body itself, has a direct influence on the organism and is involved in its metabolism, and deficiency leads to functional impairments that can only be alleviated or prevented by the trace element itself (Frieden, J Chem Educ, 1985).

Iron is the most abundant essential trace element in the human organism. The total body iron content in adults is approximately 3–5 g, distributed across functionally distinct compartments.

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2 Iron as an Essential Trace Element

Iron participates in a wide range of biological processes:

Function	Mechanism
Oxygen transport	Component of haemoglobin in erythrocytes
Oxygen storage	Component of myoglobin in muscle tissue
Energy production	Electron transfer in the mitochondrial respiratory chain (cytochromes)
Enzyme function	Cofactor of peroxidases, catalases, and other redox enzymes
Immune function	Required for proliferation, differentiation, and activation of immune cells; generation of reactive oxygen species (ROS) for pathogen killing

The dual role of iron – both essential for cellular function and potentially toxic via free radical generation – means that iron homeostasis is tightly regulated at every level, from intestinal absorption to intracellular storage.

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3 Iron Metabolism: Absorption and Distribution

Dietary Iron Forms and Intestinal Uptake

Dietary exists in the form of heme iron (meat, poultry, fish) or non-heme iron (primarily plant-based food).
In the body, iron exists in two oxidation states:

• Fe³⁺ (ferric iron): the predominant form in plant-based foods and most dietary sources
• Fe²⁺ (ferrous iron): the form preferentially absorbed by intestinal enterocytes

Because Fe³⁺ cannot be directly transported, it must first be reduced to Fe²⁺ by the brush-border enzyme duodenal cytochrome B (DcytB). Transport across the apical membrane is then mediated by divalent metal transporter 1 (DMT1).

Heme iron is transported by heme receptor - mainly HCP1 (heme carrier protein 1) - across the apical membrane and iron is released from heme by heme oxygenase.

Intracellular Storage

Within enterocytes (and other cells), surplus iron is sequestered within ferritin – a spherical protein shell that can store up to ~4 500 iron atoms in a non-toxic, bioavailable form. Ferritin thus serves as both a buffer against toxicity and a mobilisable reserve.

Basolateral Export

The export of iron from enterocytes into the bloodstream is exclusively mediated by ferroportin (FPN1), the only known iron exporter in mammals. Before iron can be loaded onto the plasma carrier transferrin, Fe²⁺ must be re-oxidised to Fe³⁺ by the ferroxidases hephaestin (at the intestinal basolateral membrane) or ceruloplasmin (in plasma).

Summary of absorption steps:

Dietary Fe³⁺  →[DcytB]→  Fe²⁺  →[DMT1]→  Enterocyte
  → stored in Ferritin  OR
  → exported by Ferroportin  →[Hephaestin]→  Fe³⁺  →  bound to Transferrin  →  circulation

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4 Iron-Containing Proteins

Iron in the body is distributed across three main pools:

Pool	Proportion	Key Proteins	Function
Functional	~74 %	Haemoglobin (erythrocytes), Myoglobin (muscle), Enzymes (cytochromes, catalases, peroxidases)	O₂ transport, O₂ storage, redox catalysis
Storage	~26 %	Ferritin, Haemosiderin	Iron reserve, buffering excess
Transport	~0.1 %	Serum iron (Fe³⁺ bound to Transferrin)	Bridge between storage and functional pool

Transferrin saturation (the proportion of transferrin binding sites occupied by iron) is therefore a sensitive marker of iron availability. Under physiological conditions, transferrin is approximately 30 % saturated, leaving substantial reserve binding capacity to buffer any transient rise in free iron.

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5 Regulation of Iron Homeostasis: Hepcidin

Hepcidin – The systemic Regulator

Hepcidin is a 25-amino-acid peptide hormone produced predominantly by hepatocytes. It functions as the major systemic regulator of iron homeostasis by inhibiting the expression of DMT1 and inactivating ferroportin:

• Inhibited DMT1-expression → Inhibition of intestinal iron absorption
• Loss of ferroportin inhibits iron export from enterocytes, macrophages, and hepatocytes
• Net result: decreased circulating iron

Regulation of Hepcidin Production

Hepcidin expression is upregulated by:

• Elevated body iron stores (via BMP/SMAD signalling)
• Inflammation – in particular IL-6 acts as the dominant hepcidin-inducing cytokine via the JAK/STAT3 pathway
• Infection (part of the hypoferraemia of inflammation, limiting iron availability for pathogens)

Hepcidin expression is downregulated by:

• Iron deficiency and anaemia
• Hypoxia (erythropoietic demand)
• Increased erythropoiesis

Relevance for Exercise

Because strenuous exercise drives an acute phase response with significant IL-6 release from contracting muscle, exercise is itself a stimulus for hepcidin elevation – transiently impairing iron absorption and mobilisation. This is the central mechanism underlying functional iron deficiency in athletes.

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6 Interactions with Other Trace Elements

Iron homeostasis does not operate in isolation. Two other essential trace elements – copper and zinc – modulate iron availability through distinct mechanisms:

Copper

Copper is required as an essential cofactor for both hephaestin and ceruloplasmin. These ferroxidases are indispensable for the Fe²⁺ → Fe³⁺ oxidation step necessary before iron can bind to transferrin.

Consequence of copper deficiency:

• Ferroxidase activity ↓ → iron cannot be loaded onto transferrin
• Iron accumulates in storage sites (ferritin, hepatocytes)
• Serum iron decreases despite normal or elevated ferritin
• Functional iron deficiency in the absence of absolute iron depletion

Zinc

Excess zinc induces synthesis of metallothionein in enterocytes. Metallothionein has high affinity for both zinc and copper; elevated metallothionein sequesters copper intracellularly and reduces its systemic availability.

Possible Consequence (evidence for the entire cascade is lacking):
Zinc excess → metallothionein ↑ → copper sequestration → functional copper deficiency → impaired ferroxidase activity → functional iron deficiency

This cascade illustrates why indiscriminate zinc supplementation without attention to copper balance can paradoxically impair iron utilisation, even when absolute iron stores are normal.

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7 Iron Deficiency in Sports

Functional Iron Deficiency

Marker	Finding
Ferritin	Normal or elevated (acute phase protein)
Serum iron	Low
Transferrin saturation	Low
Haemoglobin	Normal

Key principle: Iron is present in the body but unavailable for functional use.

Primary driver:

• Exercise-driven acute phase reaction → IL-6 ↑ → Hepcidin ↑ → ferroportin degradation and inhibited DMT1-expression → impaired iron release and intestinal absorption

Contributing factors:

• Copper deficiency or functional copper deficiency (via zinc excess → metallothionein ↑)
  → leads to impaired Fe²⁺ → Fe³⁺ oxidation (hephaestin/ceruloplasmin insufficiency)

Manifested (Absolute) Iron Deficiency

Marker	Finding
Ferritin	Low
Serum iron	Low
Transferrin saturation	Low
Haemoglobin	Low (iron-deficiency anaemia)

Manifested deficiency can develop when functional deficiency persists or is additionally exacerbated due to:

• Chronic physical training load
• Inadequate dietary iron intake (particularly in vegetarian/vegan athletes)
• Persistent low-grade inflammation
• Menstrual iron loss (female athletes)

Trajectory:

Functional deficiency (stores intact, transport impaired)
    ↓  [prolonged negative balance]
Depletion of storage reserves (ferritin ↓)
    ↓
Impaired haemoglobin synthesis (Hb ↓)
    ↓
Iron-deficiency anaemia

Understanding this continuum is critical for sports medicine diagnostics: ferritin must be interpreted in the context of CRP/inflammation status, as an acute phase response can maintain or even elevate ferritin despite depleted functional iron.

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8 Diagnostic Pathway: Stepwise Laboratory Interpretation

Iron deficiency is frequently missed in routine laboratory panels because the two most commonly requested markers — serum iron and haemoglobin — can remain within the reference range despite significant impairment of iron availability at the cellular level. A structured, stepwise approach to laboratory interpretation is therefore essential.

8.1 Why Serum Iron and Haemoglobin Are Insufficient

Serum iron reflects the momentarily circulating fraction bound to transferrin. It fluctuates substantially within the day, rises acutely after exercise-induced haemolysis, and falls only late in the deficiency cascade. Haemoglobin drops even later — only once storage and transport reserves are exhausted. A patient who is fatigued, exhausted, and lacking drive may thus present with entirely unremarkable serum iron and haemoglobin, yet harbour a clinically significant iron deficiency.

8.2 Step 1 — Measure Ferritin

Ferritin is the first-line marker for iron stores. Low ferritin is highly specific for depleted storage iron and should prompt further evaluation and intervention.

However, ferritin has a critical limitation: it is also an acute phase protein. During inflammation, infection, or strenuous exercise, ferritin synthesis is upregulated — ferritin can appear normal or even elevated despite functionally empty iron stores. A normal ferritin value in an athlete or a patient with subclinical inflammation is therefore not necessarily reassuring.

8.3 Step 2 — Assess Inflammation Status (CRP)

To contextualise the ferritin result, the C-reactive protein (CRP) should be measured simultaneously. CRP is a sensitive, rapidly responding acute phase protein and a reliable proxy for systemic inflammation.

The combined interpretation of ferritin and CRP creates four diagnostic scenarios:

Ferritin	CRP	Interpretation
↓ Low	Normal	Iron deficiency highly probable — stores depleted
Normal	Normal	Iron deficiency unlikely — stores intact, no confounding inflammation
Normal	↑ Elevated	Ambiguous — ferritin may be falsely elevated by acute phase response; stores could be depleted despite normal ferritin
↑ Elevated	↑ Elevated	Inflammatory anaemia / anaemia of chronic disease — iron trapped, not truly replete

The critical scenario is normal ferritin + elevated CRP: here, ferritin cannot be trusted as a reliable indicator of iron stores and a supplementary marker is required.

8.4 Step 3 — Soluble Transferrin Receptor (sTfR)

When the ferritin/CRP combination leaves the situation ambiguous, the soluble transferrin receptor (sTfR) provides decisive additional information.

Physiological basis: When intracellular iron availability falls below the threshold required for normal cellular function, cells upregulate surface expression of transferrin receptor 1 (TfR1) to maximise iron uptake from circulating transferrin. A proteolytic cleavage product of TfR1 is shed into the plasma, forming sTfR. Elevated sTfR therefore reflects increased cellular iron demand — indicative of iron-restricted erythropoiesis and functional deficiency at the tissue level.

Key advantage over ferritin: sTfR is not an acute phase protein and does not rise during inflammation. Its concentration is therefore unaffected by the confounding inflammatory response that renders ferritin unreliable in athletes and patients with chronic disease.

Derived index — sTfR/log(Ferritin): The Thomas plot or ferritin index (sTfR / log ferritin) integrates both markers and is the most sensitive tool for distinguishing iron deficiency anaemia, functional iron deficiency, and anaemia of chronic disease.

8.5 Integrated Diagnostic Pathway

The following decision pathway summarises the stepwise approach:

Patient symptomatic (fatigue, exhaustion, impaired performance)
│
├─ Serum iron normal AND Hb normal
│   └─ Iron deficiency NOT excluded → proceed
│
├─ STEP 1: Measure Ferritin
│   ├─ Ferritin LOW
│   │   └─ Iron deficiency highly probable (prelatent iron deficiency) → treat / supplement
│   │
│   └─ Ferritin NORMAL or ELEVATED
│       └─ STEP 2: Measure CRP
│           ├─ CRP NORMAL
│           │   └─ Iron deficiency unlikely
│           │
│           └─ CRP ELEVATED (acute phase confounding)
│               └─ STEP 3: Measure sTfR
│                   ├─ sTfR NORMAL
│                   │   └─ Anaemia of chronic disease / inflammation
│                   │       (iron trapped, not deficient)
│                   │
│                   └─ sTfR ELEVATED
│                       └─ Functional iron deficiency confirmed
│                           (cellular iron demand ↑, stores depleted
│                            despite normal ferritin)

8.6 Why Not Measure sTfR Routinely From the Start?

Ferritin remains the first-line marker because it detects deficiency earlier in the cascade — before sTfR rises (which requires progression to iron-restricted erythropoiesis). The recommended strategy is thus:

• Ferritin first — high sensitivity for depleted stores, low cost, widely available
• sTfR as second-line — resolves ambiguity when ferritin is confounded by inflammation

This two-step approach balances sensitivity, specificity, clinical utility, and cost-effectiveness (Dignass et al., J Crohn’s Colitis, 2018; Thomas et al., Clin Chem Lab Med, 2006).

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8.7 Pathway B — Confirmed Anaemia: Hb ↓ and Hkt ↓

When haemoglobin and haematocrit are both below the reference range, anaemia is confirmed. This is a distinct clinical entry point from Pathway A (which addresses pre-anaemic iron deficiency with normal Hb). Once anaemia is established, the diagnostic question shifts: what type of anaemia, and what is the underlying cause?

Step 1 — Characterise Erythrocyte Morphology: MCV and MCH

The mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH) define the morphological subtype and immediately narrow the differential diagnosis:

MCV	MCH	Morphology	Leading diagnoses
< 80 fL	< 27 pg	Microcytic hypochromic	Iron deficiency anaemia (IDA); thalassaemia trait; lead toxicity
80–100 fL	27–33 pg	Normocytic normochromic	Anaemia of chronic disease (ACD); haemolysis; acute blood loss; early mixed deficiency
> 100 fL	> 33 pg	Macrocytic	Vitamin B12 deficiency; folate deficiency; hypothyroidism; alcohol; myelodysplasia

In sports medicine, microcytic hypochromic anaemia is the dominant pattern in iron deficiency. Normocytic anaemia is common in athletes with chronic inflammation (e.g. persistent infections, IBD, post-COVID) or in the early stage of IDA before microcytosis develops.

Step 2 — Microcytic Anaemia Workup (MCV < 80 fL)

Confirm iron status with the full panel and differentiate IDA from thalassaemia trait:

Marker	IDA	Thalassaemia trait
Ferritin	↓ Low	Normal or ↑
Serum iron	↓ Low	Normal or ↓
Transferrin saturation	↓ Low	Normal
sTfR	↑ High	Normal or mildly ↑
RBC count	↓ or normal	↑ Elevated (characteristic)
RDW	↑ Elevated	Normal (uniform small cells)

Key discriminator: In thalassaemia trait, the RBC count is characteristically elevated despite low MCV (many small cells), whereas in IDA the RBC count is reduced alongside microcytosis. The Mentzer Index (MCV / RBC count) provides a simple bedside calculation: < 13 suggests thalassaemia; > 13 suggests IDA.

Step 3 — Normocytic Anaemia Workup (MCV 80–100 fL)

The normocytic pattern requires differentiation between ACD and mixed-aetiology anaemia using ferritin, CRP, sTfR, and reticulocyte count:

Marker	ACD only	IDA + ACD (mixed)	Haemolysis
Ferritin	Normal / ↑	Low–normal (masked by inflammation)	Normal / ↑
CRP	↑ Elevated	↑ Elevated	Normal
sTfR	Normal	↑ Elevated	↑
Reticulocytes	↓ Low	↓ Low	↑ Elevated
Haptoglobin	Normal	Normal	↓ Low
LDH	Normal	Normal	↑ Elevated

In athletes, normocytic anaemia with low reticulocytes, elevated CRP, and normal sTfR points to ACD (iron trapped by hepcidin, adequate stores). Mixed IDA + ACD is identified by elevated sTfR alongside elevated CRP — the sTfR signal indicates cellular iron restriction that cannot be explained by inflammation alone.

Haemolysis (exercise-induced or immune-mediated) is flagged by the triad of elevated reticulocytes + low haptoglobin + elevated LDH.

Step 4 — Macrocytic Anaemia Workup (MCV > 100 fL)

Macrocytic anaemia is less common in athletes but must not be missed, particularly in those following highly restrictive diets:

• Measure serum vitamin B12 and folate (serum and/or erythrocyte folate)
• Measure homocysteine and methylmalonic acid (MMA) for functional B12 deficiency even when serum B12 is borderline
• Screen for thyroid dysfunction (TSH)
• Consider bone marrow assessment if no nutritional cause identified

Integrated Pathway B — Confirmed Anaemia (Hb ↓ + Hkt ↓)

Hb LOW + Hkt LOW  →  Anaemia confirmed
│
├─ STEP 1: MCV + MCH
│
├─ MCV < 80 fL  (Microcytic hypochromic)
│   ├─ Ferritin ↓, TfSat ↓, sTfR ↑, RDW ↑
│   │   └─ Iron Deficiency Anaemia (IDA)  →  treat
│   └─ Ferritin normal, RBC ↑, RDW normal
│       └─ Thalassaemia trait  →  haematology referral
│           (Mentzer Index = MCV/RBC: <13 = thalassaemia, >13 = IDA)
│
├─ MCV 80–100 fL  (Normocytic)
│   ├─ CRP ↑, Ferritin normal/↑, sTfR normal, Retic ↓
│   │   └─ Anaemia of Chronic Disease (ACD)
│   │       →  treat underlying inflammation
│   ├─ CRP ↑, Ferritin normal/↑, sTfR ↑, Retic ↓
│   │   └─ Mixed: IDA + ACD  →  iron supplementation + treat inflammation
│   └─ CRP normal, Retic ↑, Haptoglobin ↓, LDH ↑
│       └─ Haemolytic anaemia
│           →  haematology referral; exclude exercise-induced haemolysis,
│              autoimmune, G6PD deficiency
│
└─ MCV > 100 fL  (Macrocytic)
    ├─ B12 ↓ / MMA ↑
    │   └─ Vitamin B12 deficiency  →  supplement / investigate cause
    ├─ Folate ↓
    │   └─ Folate deficiency  →  supplement; review diet
    └─ B12 + Folate normal
        └─ TSH (hypothyroidism), alcohol, myelodysplasia
            →  further specialist workup

Relationship Between Pathway A and Pathway B

The two pathways are sequential stages of the same iron deficiency continuum:

Normal Hb/Hkt  ←─────────────────────────────────────────── Hb/Hkt LOW
(Pathway A)                                                  (Pathway B)
Pre-anaemic:                                                 Manifest:
• Functional iron deficiency                                 • IDA
• Depleted stores + normal Hb                                • ACD / mixed
→ Act early to prevent progression                           → Characterise type,
                                                               treat cause

Early detection via Pathway A (ferritin + CRP + sTfR before Hb falls) is the preferred sports medicine strategy, as anaemia represents a late and performance-limiting stage of iron depletion.

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9 Exercise Effects on Iron Status

Short-Term (Acute) Effects

Exercise-induced haemolysis – the rupture and destruction of erythrocytes during physical exercise – is the predominant acute mechanism (Lippi & Sanchis-Gomar, Ann Transl Med, 2019):

• Mechanical trauma (foot-strike haemolysis, muscle compression)
• Osmotic and oxidative stress
• Complement activation

Haemolysis releases haemoglobin and its iron content into plasma, transiently elevating serum iron immediately post-exercise. Data from the CoSmo-S / Simon et al. (J Trace Elem Med Biol, 2026) standardised sit-to-stand test cohort confirm that serum iron is elevated immediately after exercise and increases further at 60 minutes post-exercise.

Interpretation caveat: Plasma volume contraction (hemoconcentration) also contributes to elevated post-exercise concentrations of multiple analytes; haemoconcentration correction is essential for accurate interpretation (Simon et al. 2026).

→ Interactive Dashboard – Exercise Effects on Blood & Serum Parameters

Long-Term Effects

The long-term iron response to regular training reflects competing adaptive and maladaptive pressures:

Adaptive responses (promoting iron availability):

• Erythropoietic expansion (increased O₂ delivery demand) → EPO ↑ → hepcidin suppression
• Upregulation of duodenal iron transporters in response to increased demand

Maladaptive / depleting pressures:

• Chronic hepcidin elevation from repeated IL-6 spikes (each training session)
• Cumulative haemolytic iron loss
• Sweat iron losses (minor, but significant in high-volume training)
• Gastrointestinal micro-bleeding (distance running)
• Inadequate dietary compensation

The net long-term outcome depends on training volume, nutritional strategy, and individual iron status – explaining the high prevalence of iron deficiency in endurance athletes, with estimates ranging from 15–35 % depending on sex, sport, and diagnostic criteria.

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10 Practical Implications

1. Timing of blood sampling: Serum iron, transferrin saturation, and inflammatory markers are acutely altered by exercise. Blood draws for iron status assessment should ideally be performed ≥ 24–48 h after the last strenuous session.

2. Interpret ferritin in context of inflammation: CRP should always accompany ferritin measurement. Elevated ferritin in the context of elevated CRP may reflect acute phase response rather than iron repletion.

3. Screen the full profile: The diagnostic pathway (Section 8) requires ferritin, CRP, serum iron, transferrin saturation, and haemoglobin as a minimum panel. In ambiguous cases (normal ferritin + elevated CRP), add sTfR. Single-marker screening (e.g. haemoglobin alone) misses the earliest stages.

4. Assess copper and zinc status in refractory cases: Unexplained functional iron deficiency with normal hepcidin should prompt evaluation of copper status and zinc intake, particularly in athletes using zinc supplements.

5. Dietary first: Adequate total energy intake with iron-rich foods (haem iron from meat; non-haem iron enhanced by vitamin C co-ingestion) remains the primary intervention. Supplementation should be guided by laboratory confirmation of deficiency, not symptoms alone, to avoid excess.

6. Sex differences: Female athletes, particularly in weight-sensitive and aesthetic sports, carry substantially elevated risk. Menstrual status and contraceptive history are relevant covariates in any iron assessment.

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References

• Dignass AU et al. (2018) European consensus on the diagnosis and management of iron deficiency and anaemia in inflammatory bowel diseases. J Crohn’s Colitis 12(2):238–252.
• Goddard AF et al. (2011) Guidelines for the management of iron deficiency anaemia. Gut 60(10):1309–1316.
• Looker AC et al. (1997) Prevalence of iron deficiency in the United States. JAMA 277(12):973–976.
• Thomas C, Thomas L (2002) Biochemical markers and hematologic indices in the diagnosis of functional iron deficiency. Clin Chem 48(7):1066–1076.
• Frieden E (1985) New perspectives on the essential trace elements. J Chem Educ 62(11):917–923.
• Lippi G, Sanchis-Gomar F (2019) An update on the mechanisms of exercise-induced hemolysis. Ann Transl Med 7(12):270.
• Mehri A (2020) Trace elements in human nutrition (II) – an update. Int J Prev Med 11:2.
• Puta C, Haunhorst S, Gabriel HHW (2026) Sport und Immunsystem. In: Wonisch M et al. (eds) Kompendium der Sportmedizin. Springer.
• Simon R et al. (2026) Acute effects of physical exercise on biomarkers of the trace elements selenium, zinc, copper, and iron. J Trace Elem Med Biol 94:127828.
• Zaitseva IP et al. (2018) Hepcidin and the regulation of iron metabolism. Human Physiology 44:501–509.

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One-Minute-Paper Topics

1. Define “essential trace element” in one sentence and explain why iron qualifies.
2. Name five distinct biological functions of iron in the human body.
3. Explain why dietary Fe³⁺ cannot be directly absorbed, and name the transporter responsible for intestinal iron uptake.
4. What is the role of ferroportin, and why is it described as the “only known iron exporter” in mammals?
5. Why must iron be oxidised before binding to transferrin, and which enzymes catalyse this step?
6. Describe the three iron compartments (functional, storage, transport) and give the approximate proportion of total body iron in each.
7. What is hepcidin, where is it produced, and which cytokine is its dominant upstream regulator?
8. Explain the molecular mechanism by which hepcidin reduces circulating iron levels.
9. Why does acute strenuous exercise transiently elevate hepcidin, and what are the downstream consequences for iron availability?
10. Distinguish functional iron deficiency from manifested iron deficiency using laboratory criteria (ferritin, serum iron, transferrin saturation, haemoglobin).
11. Explain how copper deficiency leads to functional iron deficiency even when iron stores are replete.
12. Trace the pathway from excess zinc intake to functional iron deficiency, naming each intermediate step.
13. Name four factors that can cause a functional iron deficiency to progress to manifested iron deficiency in athletes.
14. What is the clinical significance of measuring CRP alongside ferritin in athletes?
15. Why might a long-distance runner with “normal” haemoglobin still have impaired exercise capacity due to iron?
16. Explain the four diagnostic scenarios that arise from combining ferritin and CRP, and state what clinical action follows from each.
17. Why is sTfR not affected by inflammation, while ferritin is? Explain the physiological basis of each marker.
18. A marathon runner presents with normal ferritin (45 µg/L) but elevated CRP (12 mg/L) and performance decline. Which marker should be added, and what result would confirm functional iron deficiency?
19. When Hb and Hkt are both low, which single erythrocyte index should be checked first, and what three morphological subtypes does it reveal?
20. A normocytic anaemic athlete has elevated CRP, normal ferritin, and elevated sTfR. What diagnosis does this suggest, and how does it differ from pure ACD?