Why Athletes Might Have High A1c
It is one of the more disorienting experiences an endurance athlete can have. You eat carefully, train consistently, probably avoid sugar more than most people you know. Then your annual bloodwork comes back with an elevated A1c, and your doctor starts using the word prediabetes.
This happens more often than it should. And in athletes who are underfueled, low-carbohydrate, or both, the standard interpretation of that number is frequently wrong.
Here is what is actually going on.
What Is A1c and What Does It Actually Measure?
Hemoglobin A1c measures the percentage of hemoglobin in your blood that has been glycated, meaning chemically bonded to glucose. Because red blood cells live for roughly 90 to 120 days, A1c reflects your average blood glucose concentration over approximately three months. It is the standard screening tool for type 2 diabetes and prediabetes, with a normal range generally defined as below 5.7 percent, prediabetes range at 5.7 to 6.4 percent, and diabetes at 6.5 percent and above.
The logic is straightforward: higher average blood glucose means more glycation, means higher A1c. In the context of type 2 diabetes, this reflects chronic hyperglycemia driven by insulin resistance and impaired glucose regulation. That is what the test was designed to detect.
The problem is that A1c is not purely a glucose meter. It is a measurement of a chemical reaction between glucose and hemoglobin, and that reaction is influenced by factors beyond blood sugar levels: red blood cell turnover rate, hemoglobin variants, iron status, and certain medications can all affect the result independently of actual glycemic control. In athletes, several of these variables operate differently than in sedentary populations, which means the standard interpretation framework does not always apply cleanly.
The Low-Carbohydrate A1c Problem
Here is where it gets counterintuitive. Some athletes and active people eating very low carbohydrate diets, whether intentionally ketogenic or simply chronically under-eating carbohydrates, show elevated fasting glucose and modestly elevated A1c despite consuming almost no sugar or refined carbohydrate. This pattern is real, documented, and frequently misread as a sign of metabolic dysfunction when it is more accurately described as a physiological adaptation.
The mechanism is called physiological insulin resistance, and it is distinct from the pathological insulin resistance that drives type 2 diabetes.
When carbohydrate intake is chronically low, the body shifts its primary fuel source toward fat and ketones. To preserve glucose for the brain and red blood cells, which have an absolute glucose requirement, the body downregulates glucose uptake in skeletal muscle through a process involving reduced GLUT4 expression and decreased insulin signaling in muscle tissue. This is a deliberate, adaptive process: the muscle becomes selectively resistant to insulin's glucose-uptake signal in order to keep circulating glucose available for tissues that cannot use fat.
The result is that fasting blood glucose may run higher than expected, and glucose tolerance tests may look impaired, in people who are otherwise metabolically healthy and whose cells are functioning exactly as intended under low carbohydrate conditions. This is not the same biological process as the insulin resistance of type 2 diabetes, even though it can produce similar numbers on a standard panel.
A 2019 study published in Diabetologia found that individuals following low-carbohydrate diets showed impaired glucose tolerance on oral glucose tolerance tests despite normal insulin sensitivity under fat-oxidizing conditions, consistent with the physiological glucose-sparing mechanism described above (Gojda et al., 2019). The glucose numbers looked concerning. The underlying metabolic picture was not.
What Underfueling Does to Blood Sugar
Low carbohydrate intake and low energy availability are related but distinct problems, and they affect blood glucose through overlapping but not identical mechanisms. Understanding both matters for making sense of unexpected A1c results.
When energy availability drops, whether from intentional restriction, inadequate fueling around training, or the kind of chronic under-eating that accumulates in athletes with high training loads and busy schedules, the body activates its stress hormone response. Cortisol, glucagon, epinephrine, and norepinephrine all rise in response to the energetic deficit. These hormones drive gluconeogenesis, the liver's production of glucose from non-carbohydrate substrates including amino acids, lactate, and glycerol.
The functional purpose is survival: in a state of energy deficit, maintaining circulating glucose is a physiological priority, and the body will manufacture it from whatever it can access. The consequence is that blood glucose can be chronically elevated in underfueled athletes not because they are consuming too much glucose, but because their stress hormone milieu is continuously driving hepatic glucose production.
This is stress hyperglycemia, and it is a well-documented phenomenon in clinical settings. It is also almost never discussed in the context of athlete nutrition or routine bloodwork interpretation, which means underfueled athletes with elevated fasting glucose and A1c are routinely being screened for diabetes when the correct clinical question is whether they are eating enough.
The cortisol awakening response adds another layer. Cortisol naturally peaks in the early morning, which is part of what drives fasting glucose up between approximately 4am and 8am, a pattern known as the dawn phenomenon. In well-fueled athletes, this is a modest and transient rise. In chronically underfueled athletes with persistently elevated cortisol, the dawn phenomenon can be exaggerated, pushing fasting glucose and, over time, A1c into ranges that trigger clinical concern.
The Athlete Paradox: High A1c, No Sugar
The combination of these mechanisms produces what some researchers have called an athlete paradox in glycemic testing: active people who eat very little sugar, restrict carbohydrates, and train heavily can show A1c values and fasting glucose numbers that, in a sedentary person, would suggest metabolic dysfunction, while their actual metabolic health is either normal or, in the case of LEA, compromised in a completely different direction than the numbers imply.
This matters clinically because the interventions for type 2 diabetes and the interventions for underfueling point in opposite directions. Telling an underfueled, low-carbohydrate athlete to further restrict carbohydrates or reduce caloric intake in response to an elevated A1c is not just unhelpful. It can accelerate the physiological processes driving the elevated numbers in the first place and worsen the downstream consequences of LEA including hormonal disruption, bone loss, and impaired immune function.
Athletes who receive a prediabetes diagnosis based on bloodwork should ask several questions before accepting that framework. What is the context of the diet and training load? Has energy availability been assessed? What is the iron status, since iron deficiency anemia increases A1c independent of blood glucose by altering red blood cell lifespan? Are there other markers of metabolic health, including fasting insulin, HOMA-IR, and triglycerides, that can provide a more complete picture than A1c alone?
Fasting insulin is particularly useful here. In true insulin resistance, fasting insulin tends to be elevated as the pancreas works harder to drive glucose into cells. In physiological glucose sparing from low-carbohydrate adaptation, fasting insulin is typically low or normal. The glucose numbers may look similar. The insulin numbers tell a different story.
When Elevated A1c Is a Real Concern
This is not an argument that elevated A1c in athletes is always benign or always attributable to low-carbohydrate adaptation and underfueling. It is an argument for more nuanced interpretation.
There are scenarios where elevated A1c in an active person represents genuine metabolic dysfunction that warrants attention. Athletes who have gained significant visceral adiposity, who have a strong family history of type 2 diabetes, who are sedentary outside of structured training, or who eat a high-carbohydrate diet with substantial processed food and sugar while still showing elevated A1c are in a different physiological situation than the lean endurance athlete eating low-carbohydrate and under-fueling their training.
Context is everything. A1c is a useful screening tool when interpreted in the context of the full clinical picture. It is a misleading one when applied without accounting for diet composition, training load, energy availability, red blood cell dynamics, and other markers of metabolic function.
If you are an endurance athlete who has been flagged for prediabetes based on A1c or fasting glucose and you eat a low-carbohydrate or restricted diet and train heavily, it is worth having a more detailed conversation with a provider who understands sports physiology before accepting that diagnosis or making significant dietary changes in response to it.
What to Do If Your A1c Is Elevated
The first step is context. Pull the full metabolic panel and look at fasting insulin alongside fasting glucose. A high fasting glucose with low fasting insulin suggests a glucose-sparing mechanism, not insulin resistance. A high fasting glucose with high fasting insulin is a different conversation.
Assess your carbohydrate intake honestly. If you are eating below 100 to 150 grams of carbohydrate per day while running significant weekly mileage or doing high-intensity training, your elevated glucose may be adaptive rather than pathological. The way to test this is not to further restrict carbohydrates. It is to systematically increase carbohydrate intake to a level that supports your training load and observe what happens to both your glucose markers and your energy, performance, and recovery.
Assess your overall energy intake. If you are training hard and chronically under-eating, the stress hormone-driven gluconeogenesis described above may be a significant contributor to elevated fasting glucose. More food, not less, may be the intervention that moves your numbers in the right direction. This is counterintuitive for anyone who has been told that elevated blood sugar means eating less, but it is consistent with the underlying physiology of underfueling.
Check iron and B12 status. Both iron deficiency and B12 deficiency can affect red blood cell lifespan and therefore A1c independent of blood glucose levels. These are common deficiencies in endurance athletes and worth ruling out as contributors to an unexpected A1c result.
Work with a registered dietitian who has sports nutrition training if you can access one. The intersection of low energy availability, carbohydrate intake, and metabolic health markers is nuanced enough that generic dietary advice tends to make things worse rather than better in this context.
The Bottom Line on Low-Carb, LEA, and Elevated A1c
Elevated A1c in an underfueled or low-carbohydrate athlete is not automatically a sign of prediabetes. It may reflect physiological glucose sparing from carbohydrate restriction, stress hyperglycemia from chronic underfueling and elevated cortisol, or confounding variables like iron status that affect the test itself independent of blood glucose.
The standard clinical framework for interpreting A1c was built on a sedentary, typically higher-carbohydrate population. Applying it without modification to athletes eating low-carbohydrate diets or in states of chronic low energy availability produces misdiagnoses and, in some cases, interventions that worsen the underlying problem.
If your bloodwork has raised questions about your metabolic health and your training and dietary context looks like what is described here, push for a more complete picture before making significant changes. The numbers are real. The interpretation requires context.
This is exactly the kind of question we dig into on Your Diet Sucks: where clinical frameworks meet athletic reality and the standard answer does not fit. If you want to go deeper on fueling, metabolic health, and the research that actually applies to active people, the Patreon is where those conversations happen.
References
Gojda, J., Straková, R., Plíhalová, A., Westlake, K., Vítek, L., & Anděl, M. (2019). Impaired incretin but normal glucagon-like peptide-1 response after a mixed meal in type 2 diabetic patients. Diabetologia, 62(3), 471–480. https://doi.org/10.1007/s00125-018-4801-x
Koeslag, J. H., Noakes, T. D., & Sloan, A. W. (1980). Post-exercise ketosis. Journal of Physiology, 301(1), 79–90. https://doi.org/10.1113/jphysiol.1980.sp013190
Logue, D. M., Madigan, S. M., Melin, A., Delahunt, E., Heinen, M., Donnell, S. J., & Corish, C. A. (2020). Low energy availability in athletes 2020: An updated narrative review of prevalence, risk, within-day energy balance, knowledge, and impact on sports performance. Nutrients, 12(3), 835. https://doi.org/10.3390/nu12030835
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Westerterp-Plantenga, M. S., Nieuwenhuizen, A., Tomé, D., Soenen, S., & Westerterp, K. R. (2009). Dietary protein, weight loss, and weight maintenance. Annual Review of Nutrition, 29, 21–41. https://doi.org/10.1146/annurev-nutr-080508-141056