Why "high-carb" science is applied to the wrong athletes
In recent years, sports nutrition has entered a veritable arms race.
Carbohydrate recommendations for endurance athletes have increased from 60g per hour to 90g, and now to 120g per hour—sometimes even more. Elite marathoners and cyclists are experimenting with increasingly aggressive glucose-fructose protocols in search of marginal gains. Laboratories are publishing studies showing ever higher rates of exogenous carbohydrate oxidation.
The message amplified on social media is simple: more carbohydrates = more performance.
But performance for whom?
And for what physiological system?
What is often missing in these discussions is a crucial distinction: metabolic health is not the same as high-intensity glycolytic performance.
These systems interact.
They overlap.
But they are not interchangeable.
Confusing them leads to nutritional recommendations that may serve the elite... while undermining the metabolic resilience of the rest of athletes.
At BSE, we believe that before discussing the number of carbohydrate grams to consume at race pace, we must first understand what engine we are trying to fuel.
Three engines, not one
Human performance does not rely on a single energy system. It depends on distinct but complementary physiological engines.
The first is the lipid-dominated oxidative base, what we call the TL1 metabolic engine. It supports daily life, long basic endurance rides, and the majority of amateur athletes' training. It is mitochondrial, low-insulin, and oriented towards durability.
The second is the Aerobic Glycolytic System (AGS)—a high-flux oxidative state where carbohydrate substrate becomes predominant despite the presence of oxygen. This is the threshold zone. Marathon pace for elites. Sustained tempo efforts. Where glycogen turnover and lactate flux become critical.
The third is the oxygen ceiling system, limited by maximal cardiac output. Here, performance is constrained by stroke volume, hemoglobin mass, and oxygen transport capacity.
An athlete might have a massive aerobic base but be weak at threshold.
Another might possess an impressive VO₂max but lack durability.
A third might excel in short, intense efforts while being metabolically fragile.
Different engines.
Different limiters.
Different nutritional strategies.
Yet, modern sports nutrition often treats them as a single system.
Defining Metabolic Health
For this article, we define metabolic health as:
The ability to generate stable and high energy under different conditions, without pathological glucose dependence, excessive insulin signaling, or chronic stress activation.
This concept extends far beyond sports. It influences our daily functioning, recovery, and aging. It concerns the amateur runner training at 65% of VO₂max as much as the self-sufficient ultra-trailer in high mountains.
Metabolic health is reflected by:
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Low fasting insulin
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Stable blood sugar under stress
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High fat oxidation capacity
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Preserved mitochondrial function
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Electrolyte and hormonal stability
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Low chronic inflammation
Markers such as fasting insulin below 6 µIU/mL, a low triglycerides/HDL ratio, and reduced glycemic variability are good indicators.
Volek and Phinney's work has shown that lipid-adapted athletes can achieve fat oxidation rates above 1.5 g/min without impairing aerobic capacity (Volek et al., 2016).
Furthermore, Noakes and colleagues have questioned the classic model of glycogen depletion as the primary cause of fatigue, suggesting that exercise-induced hypoglycemia and central regulation may play a more decisive role (Noakes et al., 2023).
This does not mean carbohydrates are useless.
It means that metabolic stability—particularly the management of the "small glucose pool" (blood + liver glycogen)—is often more important than maximal muscle glycogen saturation.
A metabolically healthy human should be able to train at moderate intensity primarily on fats, tolerate nocturnal fasting without distress, and avoid energy crashes during prolonged efforts.
If one relies on a constant carbohydrate intake to survive a Zone 2 session, this reflects metabolic fragility, not physiological sophistication.
The Aerobic Glycolytic System: where carbohydrates become strategic
The Aerobic Glycolytic System (AGS) exists in another physiological reality.
It appears when ATP demand exceeds the maximum fat oxidation capacity. Glycolytic flux increases. Pyruvate dehydrogenase activity intensifies. Lactate production increases but remains compensated by its clearance.
Oxygen is present.
But it is substrate flux—not oxygen—that becomes limiting.
This is where carbohydrate availability becomes relevant for performance.
Studies by Louise Burke at the Australian Institute of Sport showed that elite race walkers adopting a low-carbohydrate, high-fat diet significantly increased their fat oxidation, but at the cost of higher oxygen consumption at race pace, impairing economy at high intensity (Burke et al., 2017).
Carbohydrates produce more ATP per liter of oxygen than fats.
At high intensity, this matters.
But at 60% of VO₂max for several hours, energy stability can be more decisive than oxygen efficiency.
The problem arises when nutritional strategies designed for the elite are indiscriminately copied by athletes whose primary limiting factor is not glycolytic flux, but metabolic resilience.
The incorrect transfer of "high carb" protocols
When a World Tour cyclist consumes 110 g/h of carbohydrates, they are operating in the Aerobic Glycolytic System for hours.
When an amateur runner at 65% of VO₂max adopts the same protocol, the physiological situation is different.
At moderate intensity, exogenous carbohydrate intake tends to almost isocalorically replace fat oxidation (Coyle et al., 1986). Performance gains are not proportional to the dose, and small amounts may be enough to stabilize blood sugar.
In already metabolically fragile individuals, chronic high carbohydrate exposure can worsen hyperinsulinemia, a condition associated with cardiovascular risk and type 2 diabetes (Kraft, 2008).
Performance does not automatically protect against metabolic dysfunction.
Why build the base before optimizing the threshold
At BSE, we recommend strengthening the metabolic engine before optimizing glycolytic flux.
This involves:
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Low-intensity volume below the first lactate threshold
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Strategic carbohydrate exposure
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Occasional reduced-glycogen sessions
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Long rides to improve hepatic glucose management
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Optimizing sodium and plasma volume
Base first.
Power second.
Conclusion
The question is not whether carbohydrates work.
The question is:
For whom?
At what intensity?
And at what metabolic cost?
The sub-two-hour marathon represents an optimization of the Aerobic Glycolytic System under elite conditions.
It is not a universal model.
Metabolic health provides resilience.
Glycolytic capacity provides speed.
The cardiovascular system provides maximal power.
Nutrition must match the engine you are training.
Build the base.
Then develop the power.
BSE — Fuel Smarter
References
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Burke, L. M., et al. (2017). Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers. Journal of Physiology.
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Coyle, E. F., et al. (1986). Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. Journal of Applied Physiology.
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Kraft, J. R. (2008). Diabetes Epidemic & You. Trafford Publishing.
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Noakes, T., Volek, J., D’Agostino, D., et al. (2023). Carbohydrate ingestion and exercise metabolism: A reappraisal of fatigue mechanisms.
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Volek, J. S., et al. (2016). Metabolic characteristics of keto-adapted ultra-endurance runners. Metabolism.
