The Two-Pool Problem

What carbohydrate is actually doing in your body — and why the elite playbook probably doesn't apply to you.

Sebastian Sawe just ran 1:59:30 in London. Three men finished under the previous world record. Coaches publicly credited 100–120 g/hr of carbohydrate. The running internet promptly lost its mind.

So on the Athlete’s Compass this week, Paul Warloski and I took the question head-on: should you be eating like Sawe?

Short answer: no. But the longer answer is more interesting. And it points somewhere the sports nutrition field hasn’t quite arrived yet.

This post is the companion piece — the figures and reading list I promised on air, plus a little more depth on the mechanism.

The two-pool model — a quick primer

Here’s the framework that Tim Noakes and colleagues lay out in their Endocrine Reviews paper, and the one I think is closest to what the data actually supports.

Figure 1. The two glucose pool model of carbohydrate metabolism during exercise. The large pool — muscle glycogen (~400–500g) — has traditionally been considered the primary fuel source and target of carbohydrate supplementation strategies. Emerging evidence suggests it functions primarily as a glucose sink, buffering circulating glucose to limit glycation and advanced glycation end-product (AGE) formation rather than serving as the principal performance determinant. The small pool — blood glucose maintained by hepatic output — fuels the brain and CNS and is the more metabolically critical target. As little as 10–20 g/hr of exogenous carbohydrate is sufficient to defend this pool and prevent exercise-induced hypoglycaemia in well-trained athletes (Prins et al., 2025; Noakes et al., 2026).

What this means practically: you need enough carbohydrate to prevent hypoglycaemia. That’s it. The dose required to do that is far lower than what elites are taking.

Phil Prins’s group showed this directly. Six weeks on a high-fat diet, six weeks on high-carb, same well-trained triathletes. In both conditions, all it took was 10 g/hr to preserve performance versus placebo. Ten. The study won AJP’s paper of the year. It’s worth your time (reference below).

The classical model said this: take more carbs, spare more glycogen, go longer. It made intuitive sense. It’s mostly wrong — and at elite doses, it may actually reverse.

Andy King’s group tested this directly, twice. In the 2018 study, ten trained cyclists rode at 77% VO₂max across five carbohydrate conditions ranging from 60 to 112.5 g/hr, with stable isotope tracers tracking exactly where fuel was coming from. Pushing the dose beyond intestinal transporter saturation — into the territory elites actually use — significantly increased muscle glycogen utilization, not reduced it (effect size = 1.68, p = 0.014). The 2019 follow-up ran the same logic over three hours: 100 g/hr burned more muscle glycogen than 90 g/hr. The authors’ own conclusion: “overdosing intestinal transport appears to increase muscle glycogen reliance.”

So at the doses being credited with world records, you’re not sparing glycogen. You’re burning more of it.

Think about why. When you flood the blood with glucose, the body has to do something with it. The muscle glycogen pool may be acting as a glucose buffer — pulling excess glucose out of circulation to protect against its toxic effects. Advanced glycation end-products (AGEs) are what happen when glucose chronically melds into your proteins. That’s accelerated ageing. Your body doesn’t want that.

There’s a real case that muscles are acting as a glucose sink first, and an energy source second. That’s a different model than the one most coaches are still working from.

The noise in the biopsy data is also worth naming. The Bergström needle technique — taking a plug of vastus lateralis and extrapolating to the whole-body glycogen store — has massive variance. Using that signal to argue for or against 90 g/hr is shakier than the confidence in those papers suggests.

So what IS high-dose carbohydrate doing?

Here’s the puzzle. If elite athletes are taking 100–120 g/hr, and increased CHO oxidation (fuel burning) doesn’t explain the performance boost, what’s going on?

Jeukendrup’s mouth-rinse studies point to the most interesting direction. Athletes who rinsed carbohydrate solution — and spat it out — showed improved performance versus placebo, with no substrate entering the body at all. Chemoreceptors in the mouth activate reward circuits in the brain. The brain reads ‘energy incoming’ and releases the brake on effort.

With frequent small concentrated doses every 10–15 minutes that athletes are doing, that signalling pathway likely stays active throughout a race. It’s not about fuel delivery. It’s about continuous CNS reassurance.

A 2:05 marathoner, when asked what he felt when the sugar hit: ‘something was unlocked.’ That’s not a metabolic description. That’s a pharmacological one.

Tim Noakes has actually asked — half seriously — whether this constitutes a pharmacological effect and whether it should be regulated. I don’t think we’re there yet. But the question isn’t ridiculous.

Figure 2 maps where the science currently sits — and where it doesn’t.

The first two pathways are established, if contested. The third is where my colleagues and I are working right now. We think there’s a mechanism connecting what the brain is doing via the oral-CNS axis to something measurable in the muscle itself — a pathway that runs in parallel to substrate and BGP defense, and that may explain a meaningful chunk of what elite athletes are actually experiencing when the carbs hit. We’re not ready to go public with the full hypothesis yet. But the figure shows you the shape of the gap we’re trying to fill. Watch the “Neuromuscular state?” box. That’s where the next piece lands.

Figure 2. Proposed pathways by which carbohydrate ingestion during exercise may improve endurance performance. Three candidate mechanisms are shown: the classical substrate/metabolic pathway (oxidation and glycogen sparing); the central/BGP defense pathway, in which oral carbohydrate sensing activates reward and motor cortex regions and blood glucose protection preserves central drive (Chambers et al., 2009; Noakes et al., 2026); and a proposed neuromodulatory pathway operating via an oral-CNS axis with downstream effects on neuromuscular state. Solid arrows indicate established mechanistic links; dashed arrows and question marks indicate hypothesised relationships requiring experimental confirmation.

What you should actually do

For age-groupers and masters athletes — the Athletes Compass audience — the evidence is pretty clear:

PRACTICAL CARBOHYDRATE TARGETS BY DURATION

< 60 min: Carbohydrate probably not needed. Water is fine.
60–90 min: 20–40 g/hr. Protecting blood glucose, nothing more.
90 min – 3 hr: 40–60 g/hr.
> 3 hr (Ironman): 50–70 g/hr. Dan Plews set the 8:18 Kona AG record on 50 g/hr.

Gut training required? Probably — whatever you’ll use on race day, practise in long training sessions. GI incidents at high doses are common and they don’t disappear without specific gut conditioning.

Note: 100+ g/hr may require months of gut adaptation. The risk of GI distress at that dose for untrained guts is real and well documented.

The broader point: every article pinning Sawe’s 1:59:30 on the carbs is underselling the 20 years of training, the coaching, the genetics, the cultural pressure to perform. The shoes and the gels are the last 1%. Don’t let them become the first thing you think about when you admire such exceptional performances.

References

Carter, J. M., Jeukendrup, A. E., & Jones, D. A. (2004). The effect of carbohydrate mouth rinse on 1-h cycle time trial performance. Medicine & Science in Sports & Exercise, 36(12), 2107–2111. https://pubmed.ncbi.nlm.nih.gov/15570147/

King, A. J., O’Hara, J. P., Morrison, D. J., Preston, T., & King, R. F. G. J. (2018). Carbohydrate dose influences liver and muscle glycogen oxidation and performance during prolonged exercise. Physiological Reports, 6(1), e13555. https://pubmed.ncbi.nlm.nih.gov/29333721/

King, A. J., O’Hara, J. P., Arjomandkhah, N. C., Rowe, J., Morrison, D. J., Preston, T., & King, R. F. G. J. (2019). Liver and muscle glycogen oxidation and performance with dose variation of glucose–fructose ingestion during prolonged (3 h) exercise. European Journal of Applied Physiology, 119(5), 1157–1169. https://pubmed.ncbi.nlm.nih.gov/30840136/

Monnier, V. M., & Cerami, A. (1981). Nonenzymatic browning in vivo: Possible process for aging of long-lived proteins. Science, 211(4481), 491–493. https://pubmed.ncbi.nlm.nih.gov/6779377/

Noakes, T. D., Prins, P. J., Buga, A., D’Agostino, D. P., Volek, J. S., & Koutnik, A. P. (2026). Carbohydrate ingestion on exercise metabolism and physical performance. Endocrine Reviews, 47(2), 191–243. https://pubmed.ncbi.nlm.nih.gov/41562187/

Prins, P. J., Noakes, T. D., Buga, A., Gerhart, H. D., Cobb, B. M., D’Agostino, D. P., Volek, J. S., Buxton, J. D., Heckman, K., Plank, E., DiStefano, S., Flaming, I., Kirsch, L., Lagerquist, B., Larson, E., & Koutnik, A. P. (2025). Carbohydrate ingestion eliminates hypoglycemia and improves endurance exercise performance in triathletes adapted to very low- and high-carbohydrate isocaloric diets. American Journal of Physiology – Cell Physiology, 328(2), C710–C727. https://pubmed.ncbi.nlm.nih.gov/39786965/

Chaudhuri, J., Bains, Y., Guha, S., Kahn, A., Hall, D., Bose, N., Gugliucci, A., & Kapahi, P. (2018). The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality. Cell metabolism, 28(3), 337–352. https://pmc.ncbi.nlm.nih.gov/articles/PMC6355252/More coming on the brain-to-muscle hypothesis when it’s ready. In the meantime, if you want the full discussion, the podcast episode is up now.

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