Don’t forget the mouth rinse with carbohydrate effect on performance.
Actually big, the whole oral microbiome is very interesting area of study, I’ve been writing a memo regarding this as a limiting factor in the nitrate pathway as some of the oral biome is responsible for fixing nitrate into nitrite.
It’s a point of personal interest as some guys were taking NO supplements dissolved in tart cherry at a stage race last year and one gentleman commented how he would brush his teeth right after to avoid staining , the research into the oral microbiome suggest that this is ironically inhibiting the effect.
That paper you link says nothing about fueling during exercise, acute lowering of LT1, insulin suppression of fat ox, insulin secretion during exercise, LT1 after a high carb meal or anything else.
It also compares literal world tour athletes (26yo) to people who exercise 2.5 hours a week (40 yo) and to people with diagnosed metabolic disorders (55yo). That gap is so wide that it would be hard to take anything out of it for ‘Recreationally trained athletes’. And even less about the acute effect of carb intake during a bike ride lowering LT1.
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You’re right that the paper doesn’t directly investigate acute carbohydrate intake during exercise or immediate post-meal shifts in LT1. It’s a cross-sectional study comparing populations with vastly different metabolic capacities, not a fueling trial.
That said, the paper documents the inverse relationship between lactate concentration and fat oxidation, and explains how elevated lactate can suppress fat oxidation both by mitochondrial substrate competition and through signaling mechanisms like GPR81-mediated inhibition of lipolysis. These pathways are well-supported by broader literature and aren’t really speculative at this point—they’re just part of the established physiology of how lactate and insulin regulate substrate use.
Crucially, even in elite endurance athletes with extremely good diabetes markers (low resistance, high sensitivity) the paper shows that fat oxidation drops off sharply once lactate exceeds around 4 to 6 mmol/L. If this suppression is measurable in athletes with exceptional mitochondrial function and lactate clearance, it stands that moderately trained individuals—and especially those with metabolic syndrome—would experience an even greater suppression under the same or lesser conditions.
So while the paper doesn’t cover all the acute effects you mentioned, some of those effects—like insulin’s suppression of fat oxidation or lactate’s inhibition of lipolysis—are already matters of public record and well-established in the literature. This paper simply helps contextualize those effects across the spectrum of metabolic fitness.
Additionally there is a whole other branch of the discussion related to latent ketosis and the effect that bolus dosing carbs can have on any overnight fasting ketosis, the presence of which will assist in fat oxidation and the reduction of which will inhibit it. This is why many people find that for an LT1 focused z2 session they will have a higher LT1 when they avoid eating carbohydrates before getting on the bike in the morning, no sugar in the coffee, no jam no toast, and very thin 30g bottles during the exercise which are sipped to reduce insulin spikes and preserve ketosis, reduce glycolytic flux and hence reduce lactate levels maximizing their LT1.
A more poignant push back would be whether or not this matters, to which I have to say I am still waiting for evidence that having an LT1 of 270 vs 260 has much of any effect on training, as we know there are many markers of racing success and having a high LT1 isn’t really one of them.