You fueled properly. A carbohydrate-rich breakfast, a gel every forty-five minutes, nothing on paper suggests today should feel this hard. And yet somewhere around hour two, your legs start negotiating with you anyway. The pace that felt automatic an hour ago now requires a decision every few hundred metres. You check your nutrition plan in your head. You did everything right. So why does your body feel like it is running on empty when your stomach is not?
The honest answer is that eating carbohydrate and actually fuelling your mitochondria with it are two different steps, and the gap between them is where a lot of good race-day nutrition plans quietly fall apart. Carbohydrate has to travel from your gut to your bloodstream, from your bloodstream into your muscle cells, and finally into the mitochondria themselves before it becomes usable energy. Each step has a ceiling. Understanding where those ceilings sit is the difference between a fuelling plan that looks right on paper and one that actually keeps your cells producing ATP for the duration of the effort.
What does carbohydrate actually become once it reaches your mitochondria?
Carbohydrate you eat is broken down into glucose, absorbed into the bloodstream, and taken up by your muscle cells, where it is either stored as glycogen or run through glycolysis, the first stage of turning glucose into usable energy. Glycolysis happens outside the mitochondria, in the main body of the cell, and produces a small amount of ATP along with a molecule called pyruvate. Pyruvate is the handoff point. It crosses into the mitochondria, where an enzyme called pyruvate dehydrogenase converts it into a form that can enter the Krebs cycle, the mitochondrial process that strips electrons from your fuel and feeds them into the electron transport chain, the final stage that generates the overwhelming majority of the ATP your muscles actually spend during sustained effort. This is why mitochondrial capacity and carbohydrate availability are not competing explanations for fatigue. They are two halves of the same supply chain, and a shortfall in either one produces the same felt result: your legs slowing down while your mind is still willing.
Why does carbohydrate matter more at some intensities than others?
Your body runs on a blend of carbohydrate and fat at almost every intensity, but the ratio shifts sharply as effort increases. At an easy, conversational pace, fat oxidation can supply a large share of your energy needs, and your mitochondria can sustain that output for hours with comparatively modest carbohydrate input. Push into tempo or threshold intensity, and the equation changes. Fat oxidation, while metabolically efficient, cannot deliver ATP fast enough to meet the demand of harder efforts, so your body leans more heavily on carbohydrate to keep pace with the electron transport chain's appetite for fuel. This is the part that catches a lot of well-intentioned athletes off guard. A rider who fuels adequately for a steady endurance pace, then surges for a climb or a breakaway, is asking their mitochondria to process carbohydrate at a rate their glycogen stores and blood glucose delivery may not be able to sustain, even if the total calories consumed that day were technically enough.
Layer one, two, and three: where does a fuelling shortfall actually happen?
When athletes talk about "running out of fuel," they are usually describing one of three distinct bottlenecks, and telling them apart matters because the fix is different for each.
Layer 1: Muscle glycogen depletion. Your muscles store a limited amount of glycogen, typically enough for somewhere between 90 minutes and two hours of moderate to hard effort, depending on your fitness, diet, and the specific muscles involved. Once local glycogen runs low, that muscle has less readily available fuel to hand off to its own mitochondria, regardless of what is happening elsewhere in your body.
Layer 2: Blood glucose delivery. Even with glycogen still in reserve, your body needs to keep blood glucose available to support ongoing carbohydrate oxidation, particularly once local stores start running thin. This is the layer your on-course fuelling, gels, drinks, chews, is designed to support directly, since it replenishes the bloodstream pool your muscles continue to draw from.
Layer 3: Mitochondrial oxidation capacity. This is the layer most fuelling advice ignores entirely. Even with abundant glucose available, your mitochondria can only process it as fast as their density and functional capacity allow. A well-trained athlete with high mitochondrial density can extract more ATP from the same carbohydrate intake than a less-trained athlete doing the identical effort, which is part of why fitness itself functions as a fuelling advantage, not just a cardiovascular one. A fuelling problem at layer one or two is usually a nutrition and timing fix. A limitation at layer three is a training and cellular-support problem, and it is the one that gets the least attention despite being just as real.
How can you tell which layer is actually limiting you?
The pattern of the fatigue is the clue. A sudden, sharp crash, the classic bonk, where pace collapses abruptly and mental fog sets in quickly, points toward layers one and two: glycogen and blood glucose running genuinely low, often correctable within twenty to thirty minutes of taking in carbohydrate. A slower, more gradual erosion, where pace drifts down over an hour or more despite steady fuelling intake, and where a gel or a sports drink does not produce the quick rebound a true bonk usually responds to, points more toward layer three. Your body has the fuel. It is struggling to convert it fast enough. This distinction matters practically: an athlete who keeps eating more carbohydrate to fix a layer-three limitation is treating the wrong problem, and often ends up with gut discomfort on top of unresolved fatigue. Athletes who train consistently at the intensities they race tend to develop a reasonably accurate internal sense of which pattern they are experiencing over time, though it takes deliberate attention to notice the difference rather than labelling every hard patch as the same generic bonk.
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What actually happens to ATP production when carbohydrate availability drops?
When blood glucose and glycogen both run low, your mitochondria do not simply stop. They shift their fuel mix toward fat oxidation and, in prolonged deficit, toward protein breakdown, but neither substitute matches carbohydrate's ability to feed the electron transport chain fast enough to sustain a hard pace. The practical result is a drop in maximum ATP output precisely when your muscles are asking for more of it, not less.
Research on exercise-induced oxidative stress shows that this kind of metabolic strain, particularly under prolonged, glycogen-depleted conditions, also increases reactive oxygen species production in working muscle, adding oxidative load on top of the fuel shortfall itself. In other words, running low on carbohydrate does not just slow your energy production down. It can compound the cellular stress your mitochondria are already managing from the effort itself, a double cost that is easy to underestimate from the outside. This is also part of why chronic under-fuelling, not just a single bad race, matters for long-term mitochondrial health. Athletes who repeatedly train in a depleted state without adequate recovery nutrition are asking their mitochondria to operate under compounding oxidative pressure, which affects the biogenesis process, the mechanism by which your body builds new mitochondrial capacity in the first place. Consistent underfuelling can work against the very adaptation endurance training is supposed to produce.
Does training actually change how efficiently your mitochondria use carbohydrate?
Yes, and this is one of the more useful long-term implications of consistent endurance training. Mitochondrial biogenesis, the process of building new mitochondria in response to training stimulus, increases not just the number of mitochondria available but the efficiency with which existing ones convert pyruvate into ATP. A well-trained athlete extracts more usable energy from an identical carbohydrate intake than a less-trained athlete performing the same effort, which is one reason experienced endurance athletes often report needing less on-course fuelling, proportionally, than they did earlier in their training history, even at similar or faster paces. This does not mean carbohydrate intake becomes less important as fitness improves. It means the ceiling on what your body can do with that carbohydrate rises, which is a genuinely different mechanism than simply getting better at pacing or tolerating discomfort. The cellular machinery itself becomes more capable.
Can you train your mitochondria to rely more on fat and spare your carbohydrate stores?
To some extent, and this is where "fat adaptation" training strategies come from, though the practical benefit is narrower than some of the marketing around it suggests. Consistent training at easy, fat-oxidation-dominant intensities does increase your mitochondria's capacity to draw on fat as fuel, which can modestly extend how long your glycogen reserves last at a given easy pace. What this adaptation does not do is meaningfully raise the ceiling on how much power or pace you can sustain at hard, carbohydrate-dependent intensities. A fat-adapted athlete still needs adequate carbohydrate to sustain a threshold effort or race pace, since fat oxidation simply cannot supply ATP fast enough to meet that level of demand, regardless of how well-trained the fat-oxidation pathway has become. Fat adaptation is a tool for extending easy-effort endurance, not a substitute for carbohydrate at the intensities where most races are actually decided.
What supports your mitochondria's ability to actually use the fuel you give them?
Fuelling strategy addresses layers one and two, glycogen and blood glucose. Supporting layer three, the mitochondria's own capacity to process that fuel, is a different and often neglected piece of the picture, and it is not something you can fix with a gel mid-race. It is built and protected between sessions, through training consistency and through the cellular environment you maintain day to day. Oleuropein, the primary polyphenol in olive leaf extract, has been studied specifically for its role in supporting mitochondrial calcium handling and function, a process directly involved in how efficiently mitochondria convert available fuel into ATP.
Research on oleuropein's effect on mitochondrial bioenergetics during moderate-intensity exercise in humans found measurable improvements in how muscle mitochondria responded to a training stimulus, which is a mechanistically different lever than fuelling timing altogether. Micronutrient adequacy plays a supporting role too. Magnesium acts as a cofactor in ATP synthesis itself, meaning a genuine deficiency does not just cause cramping or poor sleep, it can directly limit how efficiently your cells convert available fuel into usable energy. B vitamins play similar cofactor roles across the metabolic pathways that move glucose from your bloodstream into mitochondrial ATP production. None of these compensate for genuinely inadequate carbohydrate intake. What they do is support the conversion step that fuelling alone cannot address, which is the layer most nutrition plans leave completely unmanaged.
Does the type of carbohydrate change how efficiently your mitochondria can use it?
To a meaningful degree, yes, though the differences show up more in digestion speed and gut comfort than in the mitochondria's ability to process the fuel once it arrives. Glucose and maltodextrin are absorbed quickly and reach the bloodstream in a form your muscles can use with minimal additional conversion. Fructose follows a different absorption pathway through the liver, which is part of why blended glucose-fructose formulations, common in modern sports nutrition products, allow for higher total carbohydrate absorption rates during exercise than glucose alone, since the two sugars do not compete for the same transport mechanism in the gut. Once carbohydrate has actually reached your muscle cells and been converted to pyruvate, your mitochondria do not meaningfully distinguish which specific sugar it originated from. The practical takeaway is that carbohydrate source matters most for how much you can comfortably absorb and how quickly, not for what happens once it reaches the electron transport chain itself.
How does chronic training volume change your body's relationship with carbohydrate?
High training volume over months and years produces a genuine adaptation in how your body manages carbohydrate, not just in how efficiently your mitochondria use it in a single session. Consistent endurance training increases the density of glucose transporters in muscle cell membranes, improving your capacity to move glucose out of the bloodstream and into the cell in the first place, a step upstream of the mitochondria that is easy to overlook. Training also improves glycogen storage capacity itself, meaning a well-trained athlete can store more usable fuel per kilogram of muscle than an untrained person eating an identical diet. This compounds with the mitochondrial efficiency gains discussed earlier: a trained athlete both stores more fuel and converts it more efficiently once it reaches the mitochondria, which is part of why the same relative effort feels dramatically more sustainable after a year of consistent training than it did in month one.
Where does the Daily Shot fit into this picture?
The Daily Shot combines oleuropein, magnesium, vitamin B6, and vitamin C, taken once a day, to support the mitochondrial side of the fuelling equation, the layer that determines how efficiently your cells actually use the carbohydrate you eat, rather than how much carbohydrate you consume in the first place.
It is not a race-day fuelling product and does not replace your gels, drinks, or on-course nutrition plan. It is a daily foundation, built to support the cellular machinery so that when you do fuel properly on race day, your mitochondria are positioned to make full use of it.
In a placebo-controlled trial with 28 World Tour professional cycling team riders, the OLEUS protocol was associated with better maintained power output over a multi-day endurance test, with the clearest separation from placebo emerging in the later stages, when fatigue resistance and fuel efficiency become decisive. That result sits alongside, rather than instead of, the published research on oleuropein and mitochondrial function summarised above.
Feed the machinery, not just the tank
The Daily Shot supports the mitochondrial side of fuelling, the layer that determines how well your cells use the carbohydrate you already eat.
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Sources
Gherardi, G., et al. (2024). Mitochondrial calcium uptake declines during aging and is directly activated by oleuropein to boost energy metabolism and skeletal muscle performance. Cell Metabolism. PubMed search
Lanfranchi, C., et al. (2026). Oleuropein-based olive leaf extract enhances muscle mitochondrial bioenergetics response to moderate but not maximal intensity exercise in humans. Journal of Physiology. PubMed search
Jeukendrup, A.E. (2014). A step towards personalized sports nutrition: carbohydrate intake during exercise. Sports Medicine, 44(Suppl 1), S25-S33. PubMed: 24791914
Powers, S.K., Radak, Z., Ji, L.L. (2016). Exercise-induced oxidative stress: past, present and future. Journal of Physiology, 594(18), 5081-5092. DOI: 10.1113/JP270646
Hood, D.A. (2009). Mechanisms of exercise-induced mitochondrial biogenesis in skeletal muscle. The Journal of Physiology, 587(23), 5527-5539. PubMed: 19448716
Nielsen, F.H., Lukaski, H.C. (2006). Update on the relationship between magnesium and exercise. Magnesium Research, 19(3), 180-189. PubMed search
Kerksick, C.M., et al. (2017). International society of sports nutrition position stand: nutrient timing. Journal of the International Society of Sports Nutrition, 14, 33. PubMed: 28919842
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