HbA1c in Athletes: Why Your Blood Sugar Marker May Be Misleading You
Table of Contents
Introduction
I often see HbA1c treated as a straightforward marker of blood sugar control. In athletes, however, the picture can be more complicated. Depending on the clinical context, HbA1c may appear unexpectedly high or unusually low, even when the athlete’s overall metabolic profile does not clearly suggest diabetes.
This matters because HbA1c — glycated hemoglobin — is one of the most widely used markers in clinical medicine. It is used to diagnose prediabetes and diabetes and to monitor long-term glycaemic control. Standard reference ranges classify an HbA1c of 5.7–6.4% as prediabetes and ≥6.5% as diagnostic for diabetes [9]. These thresholds are based on general-population data, not athlete-specific physiology [9].
In trained individuals, I do not interpret HbA1c in isolation. I look at the result alongside fasting glucose, symptoms, body composition, training history, iron status, and other laboratory findings. Many highly trained athletes have a lower overall risk profile for type 2 diabetes than sedentary populations, but type 2 diabetes can still occur when additional risk factors are present. Type 1 diabetes can also occur in athletes and should never be dismissed simply because someone is fit or highly active.
This article explains why HbA1c can be misleading in athletes, how exercise-induced haemolysis and iron deficiency can shift the result in opposite directions, and how to interpret HbA1c more accurately in the context of a trained body.
What HbA1c Actually Measures — and Why Athletes Are Different
HbA1c in athletes reflects the same process as in everyone else: the glycation of haemoglobin, where glucose binds irreversibly to haemoglobin molecules within red blood cells (RBCs) over time. The conventional assumption is that RBCs have a lifespan of approximately 90 to 120 days, and that HbA1c therefore indicates the mean blood glucose concentration over the lifespan of the RBC [1].
HbA1c is part of the basic laboratory panel I use in athletes, much as it is in the general population. It is one of the core markers I follow when assessing vascular and metabolic risk, and I measure it regularly during routine follow-up visits.
In practice, HbA1c is often measured together with fasting glucose. In many clinical settings, this has reduced the need for routine oral glucose tolerance testing, because HbA1c provides a convenient estimate of longer-term glycaemic exposure. However, oral glucose tolerance testing remains important when clinically indicated, particularly when HbA1c and fasting glucose do not provide a clear answer.
In Finland, oral glucose tolerance testing is also still commonly used during pregnancy, where screening for gestational diabetes follows its own clinical pathway.
In athletes, certain physiological factors can alter RBC lifespan and thereby affect how accurately HbA1c reflects true glycaemic status. Research in a small study of six diabetic subjects and six non-diabetic controls found that RBC lifespan varies substantially across individuals — even among those who are hematologically normal — and that this variation was large enough to cause clinically important differences in HbA1c for a given mean blood glucose [2]. In other words: two people with identical average blood glucose levels can have meaningfully different HbA1c values simply because their red blood cells age at different rates.
In athletes, two physiological mechanisms can shift HbA1c in opposite directions relative to true glycaemic status. Understanding both can improve interpretation of HbA1c in athletes. If you are not sure how to prepare your blood tests as an athlete to get the most reliable results, read my guide on preparing for blood test athletes.
Mechanism 1: Exercise-Induced Hemolysis — HbA1c in Athletes Can Read Falsely Low
Exercise-induced hemolysis can involve the rupture and destruction of red blood cells through multiple proposed pathways: direct compression of RBCs during foot strike (particularly in running), repeated muscle contractile activity, vasoconstriction in internal organs, and metabolic abnormalities developing while exercising including hyperthermia, dehydration, lactic acidosis, shear stress, and oxidative damage [3]. I have covered the clinical presentation of this in detail in my article on footstrike hemolysis.
The clinical significance is substantial. A 2019 review in Annals of Translational Medicine, citing earlier erythrocyte-survival work [7], reported that erythrocyte lifespan in runners is approximately 40% shorter than in sedentary controls [3]. If the assumed RBC lifespan underpinning standard HbA1c interpretation is ~120 days, a 40% reduction would correspond to approximately 70–80 days. Because increased RBC turnover can reduce the average exposure time of circulating RBCs to glucose, HbA1c may be biased downward in runners with evidence of increased RBC turnover relative to glucose measurements.
Exercise-induced haemolysis is also commonplace — not exceptional. The same review reported that a substantial degree of exercise-induced haemolysis can occur after short-, medium-, long- and ultra-long distance running, with severity depending on the athlete population, analytical technique, and the number, frequency, and intensity of ground contacts [3].
In clinical practice, I usually treat this as an interpretive finding rather than a major diagnosis in itself. A 2024 scoping review of long-distance runners found that changes in reticulocyte count and haptoglobin suggested transient foot-strike haemolysis, while haemoglobin and haematocrit did not change notably [10]. Similarly, after a 60-km ultramarathon, reduced haptoglobin suggested haemolysis, but the overall degree of red cell injury was described as very modest or clinically negligible [11].
This matches how I usually see it in practice: foot-strike haemolysis is often a supporting clue rather than the main clinical problem. I rarely use it alone to make major treatment decisions, but I do consider it when HbA1c seems unexpectedly low compared with fasting glucose or the athlete’s broader clinical picture.
Markers such as haptoglobin in athletes and, in some contexts, bilirubin in athletes may help assess haemolysis when interpreted with the full clinical picture. In a runner with evidence of haemolysis or increased RBC turnover, HbA1c may be lower than expected relative to glucose measurements.
Mechanism 2: Iron Deficiency — HbA1c in Athletes Can Read Falsely High
Iron deficiency is frequent among athletes, with higher rates observed in female athletes and endurance disciplines [8]. It creates a physiologically opposite HbA1c distortion. For a full overview of iron status assessment, see my article on iron panel interpretation for athletes.
A 2015 systematic review in Diabetologia — examining 12 articles drawn from MEDLINE, EMBASE, CINAHL, and the Cochrane Library — found that the presence of iron deficiency with or without anaemia led to an increase in HbA1c values compared with controls, with no concomitant rise in glucose indices [4]. This pattern is consistent with a spurious HbA1c elevation rather than true hyperglycaemia.
One proposed explanation involves altered erythrocyte turnover, which may increase the time available for haemoglobin glycation. Iron deficiency and IDA may increase HbA1c without a corresponding rise in glucose indices, likely through effects on erythrocyte turnover and erythrocyte indices [4]. The systematic review noted that iron deficiency, as well as iron deficiency anaemia (IDA), may be sufficient to cause a change in HbA1c values, which is highly relevant in women of childbearing age [4] — a group that includes a substantial proportion of female athletes. For a comprehensive overview of blood markers specific to female athletes, see my guide on female athlete bloodwork.
When evaluating iron-related erythrocyte changes, RDW in athletes — red cell distribution width — is worth reviewing alongside other red cell indices.
The clinical implication is usually subtle rather than dramatic. In my experience, the effect of iron deficiency on HbA1c is often small enough to go unnoticed, especially because many athletes have a low overall risk profile for type 2 diabetes and their HbA1c often remains within the reference range. For that reason, I rarely treat this as a stand-alone finding. I pay more attention to it when HbA1c is borderline, rising over time, or does not fit with fasting glucose, iron status, training history, or the athlete’s broader clinical picture.
I also think it is important to remember that this is not truly athlete-specific. Iron deficiency can affect HbA1c interpretation in anyone. The reason I consider it particularly relevant in sports medicine is that iron deficiency is relatively common in athletes, especially in female athletes and endurance disciplines [8]. For the performance thresholds that actually matter, see my article on ferritin levels for athletes.
What the Data Show on HbA1c in Athletes
The divergence between fasting plasma glucose and HbA1c in athletes was formally quantified by Lippi and colleagues in a study published in the International Journal of Sports Medicine in 2008. The study population consisted of 47 male professional road cyclists, 72 male elite road cyclists, and 58 male sedentary blood donors [5].
A significant difference was observed for fasting plasma glucose (FPG) between sedentary controls (96 ± 8 mg/dL) and either elite (91 ± 8 mg/dL; p < 0.001) or professional cyclists (89 ± 8 mg/dL; p < 0.001) [5]. Athletes had lower fasting glucose — compatible with training-related differences in glucose metabolism, though the study did not directly measure the mechanism.
Yet HbA1c moved in the opposite direction. Athletes showed a consistent trend towards higher HbA1c values, reaching statistical significance between sedentary individuals and professional cyclists (5.2 ± 0.3% versus 5.4 ± 0.2%; p = 0.017) [5]. In multiple linear regression analysis, the intensity of physical exercise was inversely correlated with FPG (r = −0.320; p < 0.001) and directly correlated with HbA1c (r = 0.190; p = 0.006) [5].
This dissociation — lower fasting glucose paired with higher HbA1c — may complicate standard interpretation if HbA1c and fasting glucose are considered without training context, and highlights the need for establishing appropriate reference values for HbA1c in athletes according to training workload [5]. Note that this study was conducted in male cyclists only; generalisation to other athlete populations should be made with appropriate caution.
In clinical practice, the HbA1c effect of iron deficiency is usually modest, and it is not something athletes need to be overly worried about on its own. Many highly trained athletes have a generally favourable risk profile for type 2 diabetes, so small shifts in HbA1c often remain within the reference range and do not trigger major clinical action.
Type 1 diabetes is different. When type 1 diabetes develops, the presentation is often more acute, and the diagnosis is usually driven by clearly elevated blood glucose rather than a subtle HbA1c change. Athletes with new-onset type 1 diabetes may present with symptoms such as excessive thirst, frequent urination, unexplained weight loss, fatigue, nausea, abdominal pain, or rapid breathing. These symptoms should prompt immediate glucose and ketone assessment rather than reassurance based on athletic fitness or training status.
Conclusion
HbA1c is part of standard metabolic screening, but in athletes it is often less informative than it first appears. I still measure it, because it can help identify broader glycaemic risk and it is widely used in routine care. But in trained individuals, I rarely interpret HbA1c as a decisive marker on its own.
The reason is simple: HbA1c is not just a glucose marker. It is also affected by red blood cell lifespan, exercise-related red cell turnover, iron status, and sometimes the timing of blood collection. Exercise-induced haemolysis may bias HbA1c downward in athletes with increased red cell turnover, while iron deficiency may push HbA1c upward without a true rise in glucose. In most athletes, these effects are subtle, but they can still make the number harder to interpret.
In clinical practice, I pay most attention to HbA1c when it is clearly abnormal, rising over time, or inconsistent with fasting glucose, symptoms, body composition, training history, or iron markers. A mildly borderline HbA1c in a well-trained athlete should not automatically lead to a diabetes label, but it should prompt a more careful look at the whole picture.
At the same time, athletic fitness should not create false reassurance. Type 2 diabetes is less common in many highly trained athletes, but it can still occur when risk factors are present. Type 1 diabetes can also occur in athletes, and a new presentation is usually driven by clear symptoms and high glucose rather than a subtle HbA1c change.
The practical takeaway is that HbA1c in athletes is a screening tool, not a final answer. It belongs in the panel, but it needs context. For many athletes, fasting glucose, symptoms, training load, iron status, and repeat trends often tell me more than a single HbA1c value.
References
[1] https://www.ncbi.nlm.nih.gov/books/NBK470185/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC2581997/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC6614330/
[4] https://pubmed.ncbi.nlm.nih.gov/25994072/
[5] https://pubmed.ncbi.nlm.nih.gov/17614026/
[6] https://pubmed.ncbi.nlm.nih.gov/29884709/
[7] https://pubmed.ncbi.nlm.nih.gov/1653657/
[8] https://pubmed.ncbi.nlm.nih.gov/26512429/
[9] https://pmc.ncbi.nlm.nih.gov/articles/PMC2699715/
