My recollection is that Nate (and some of the other hitters, like Keegan Swenson) only does this in the window leading into a long race like Leadville, or during a stage race.
I wish they had made this point clear on the podcasts. Well said!
What is it caused by?
Very interesting thread here… I have a strong familial history of T2D. I’ve been quite concerned about fueling when cycling and typically only have gels when I train or cycle.
I do note significant blood sugar spikes but these come down within 30 mins of intense exercise.
From what folks have posted here, I don’t have much to worry about. My last HBA1C was at the top end of normal (I have confirmed impaired fasting glycaemia).
I rode a long event yesterday 120mi / 10.8k climbing. Took me about 7 hours, I fueled with 6x80g Beta Fuel + 2 Clif bars + 3 Maurten 100 + 2 bags Clif Bloks, in 7 bidons of water. I ate a PBJ sandwich for breakfast with coffee at 4:30am. Event started 6:45am and I finished around 2pm.
I found myself in an extreme sugar high for hours after the event. Around 7pm it was uncomfortable. I craved veggies and avocado even though my wife had made lasagna.
I’m now wondering if I should have continued to ride to clear the sugar high.
In what form is the 120g/h?
Yeah they should caveat it a bit, especially the large human Nate (@stevemz that really made me laugh!)
Just revisited this thread as a result of a comment above. I am that person and up until now haven’t been consuming anything like 60g/hour except on long hard group rides. However I looked at an old 2018 metabolic test I had done and discovered that at my endurance power my efficiency was WAY down at 18% and only got to to 20+% on supra threshold wattages. This despite have a presumably reasonable FATMAX of 0.75=-0.80 g/min at those power levels. Doing some maths has shown that this makes a massive difference to how much more CHO I should consume on a ride. I’m going to up my intake and see if it improves not only my performance but also my recovery which seems to have gotten worse over the last year to or so.
The other day my wife noticed how I was preparing my skratch drink mix (ie. Adding scoop after scoop of the white drink mix to my water bottles), and she voiced a concern that all these high carb/sugary sport fuel products I consume, could be putting stress on my body, which might lead to type 2 diabetes.
I dismissed her concern, and explained that because I am burning through so much of those carbs/sugar when I ride, I don’t have anything to worry about. But am I right about that? I mean, I do consume a lot of energy gels, cliff bars, ounces of skratch/Gatorade mix, and various other sport fuel products, but at the same time, I train a lot too.
Perhaps us cyclists, and endurance athletes in general, who consume far more sugar than might otherwise be recommended, aren’t at risk of developing insulin resistance. But, could all these products be putting us at risk of some other gut ailment or nutritionally induced health issue?
I don’t think there are long term robust studies that show endurance athletes are immune to T2D. I know there is evidence that short term use is fine.
Somebody share with me the study if there is one. I think it’s just anecdotal.
I don’t think just because you’re exercising that you can drink sugar with impunity. However, it has a big effect on performance for endurance exercise, so the benefit outweighs the cost in the short run
Aside from what you “think,” what physiologic basis do you have for this statement?
Know what plays perhaps the biggest role in development of T2DM?
Genetics. First degree relatives of someone with T2DM have 5-10x the risk of developing T2DM compared to age/weight-matched controls.
I’m afraid this is just not correct. Glut4 requires insulin.
T1Ds decrease insulin because the work of cycling burns glucose, not because glucose magically gets into the cells - insulin is still required to open the cellular absorption pathway.
I would caution against saying everyone can drink sugar with reckless abandon and no one can drink sugar at all. We’re all different and have different physiology. I for example am prediabetic. I only have carbs / sugar when I’m cycling, rest of the time I’m zero carb. Cycling friends I know are able to consume sugar that would make me diabetic, whilst maintaining low HBA1Cs.
We’re all different. Best thing you can do is to have an impaired fasting glycemia test and an HBA1C and see where you are on the metabolic spectrum.
Where, then, is the glucose burned if not in the cells? Just going poof! in the blood?
No, it doesn’t require insulin. GLUT4 translocation is indeed stimulated by insulin. Insulin binds to the insulin receptor on the cell membrane, which dimerizes and catalyzes a signaling cascade whose net result is insertion of the GLUT4 transporter into the cell membrane. GLUT4 allows facilitated diffusion of glucose into the cell. The diffusion itself does not require insulin.
Muscle contraction (skeletal, cardiac) can, independent of insulin, cause insertion of the GLUT4 transporter into the cell membrane. Thus, glucose can be brought into the cell.
Unless this study actually correlates certain genes, the narrative just as validly suggests that nurture rather than nature plays the biggest role in development of T2DM. For example, mom and dad got fed junk by grandparents. They have the habit of eating junk. Raise their kids eating junk. Everyone develops T2DM. T2DM is considered a ‘lifestyle disease’.
Perhaps eating high amounts of sugar in a bike somehow has no direct effect on long term health. However, few people can consume high amounts of sugar without having it affect the palate. Few people can consume sugar only while on the bike. I imagine these people would develop T2DM in the long run. Some outlier elite athlete may not, but a typically weekend warrior hobby cyclist likely will
…Genetics of type 2 diabetes - PMC
Type 2 diabetes (T2D) is the result of interaction between environmental factors and a strong hereditary component.
Highly replicated genes, for example TCF7L2, KCNQ1 and KCNJ11, are discussed in greater detail. Taken together, the genetic loci discovered to date explain only a small proportion of the observed heritability.
Type 2 diabetes has a higher genetic risk than type 1 diabetes which is an autoimmune disease to put it in context
This is the punchline to that literature review:
“ While we know that a person’s future risk of developing T2D has a significant heritable component and believe that most of this inherited risk is associated with particular genotypic features (in most cases, multiple variants of small effect?), and have identified several risk variants in genome-wide association studies, these variants still explain a relatively small proportion of the observed heritability. Several studies have found that a risk score based on traditional risk factors (BMI, family history, age, sex, HDL, triglycerides, etc .) consistently outperforms any set of genetic markers and the addition of known genetic markers does not significantly improve prediction based on traditional risk factors[81-83].”
It seemed that many genes have been correlated but they never mention the extent to which their presence explains incidence of T2DM (because it is negligible). It is easy to find a statistically significant effect in science. It’s much harder to find one with a magnitude that is clinically meaningful. Sociodemographic and lifestyle factors currently do so given the state of the literature.
I mean…you jumped straight to this conclusion. The vast majority of people who consume high levels of sugar never develop T2D, and the number of athletes with T2D is even lower. If we are discussing relative risk, there is no known clinically meaningful data that shows that it is risky for athletes to consume high levels during exercise. If there is, I’d love to see. it.
I highly doubt the average person would read that statement you quote above and feel that it is a jump to a conclusion. Though, I do think the conclusion is logical. Feel free to experiment and prove it wrong. I hope you stay T2DM free! Lol
Several studies have found that a risk score based on traditional risk factors (BMI, family history, age, sex, HDL, triglycerides, etc .) consistently outperforms any set of genetic markers and the addition of known genetic markers does not significantly improve prediction based on traditional risk factors[81-83].”
It is not surprising that “traditional risk factors” which include genetics indirectly (through family history) are not improved by adding genetic markers. You’ve basically already controlled out the effect.
Furthermore, the study showing that genetics was a large factor already controlled for age and weight, which are other known factors.
Anyway, consumption of sugar while exercising is definitely not a “traditional risk factor”. One of the studies you refer to has two such lists: Cambridge (age, sex, drug treatment, family history of type 2 diabetes, body mass index, smoking status) and Framingham (age, sex, parental history of type 2 diabetes, body mass index, high density lipoprotein cholesterol, triglycerides, fasting glucose). Neither has any dietary component. If consumption of sugar while exercising doesn’t spike your insulin levels (for reasons given above), and doesn’t cause weight gain (because you’re burning the calories at least as fast as you’re taking them in), there’s no obvious mechanism for it to cause Type 2 diabetes. And this applies to the weekend warrior as much as the top athlete, as long as the WW is not gobbling gels while sitting on the couch.
Kind of. But kind of also not quite. Cellular insulin sensitivity is 50x higher during exercise. Magnitude of insulin response in non-T1D folks is miniscule during exercise compared to outside of exercise.
This is important.
There is currently an over-application of T2D & T1D info to non-diabetics in the field of sport nutrition.
There isn’t. And there is serious physiological mechanistic reason to believe that people with blood sugar dysregulation can indeed consume high levels of sugar during exercise and pose no risk of pancreatic damage.
As an anecdote, this past spring I consumed 300-700g of sugar per day for almost a month and ended up with an a1c of 4.9.
If there were risk, my wife and I, and probably @brendanhousler would have extremely high likelihood of being diabetic by now. As a great sport science professor of mine usually asked when folks asked about health risks where there were none, “where are the bodies!?!” (as in, where are the bodies of athletes dropping dead from T2D). Yes, it’s totally crass, and insensitive and inappropriate but it highlights an important point:
Where there is risk, there will be some correlation, at least. There isn’t here.
PS. don’t ask my wife about her dental health.
Couldn’t have said it better myself. Saving this response!