It’s kind of a slow night in the NFL, so I’m half-assedly digging around the internet for data on alcohol metabolism and ketogenic fat loss.
Basically, my premise is that alcoholic ketoacidosis is a thing, and is both related to ketosis and physiologically different from other forms of ketoacidosis, so maybe there are ways to use it to my advantage. I had a vague notion going in that alcohol consumption — in particular, the hard stuff, rather than maltose-laden beer — somehow speeds up the transition to ketosis after a carb load. If it does so by depleting liver glycogen, a few stiff drinks would act as a cheat code to get deep into ketosis after a depletion workout.
Unfortunately, most of what you get if you google up “alcohol metabolism” is variations on the theme of “OH WOW YOU GUYS, DID YOU KNOW THAT DRINKING TOO MUCH IS BAD FOR YOU? SOME VERY SMART PEOPLE IN WHITE COATS SAID SO, BECAUSE SCIENCE! (No, we won’t tell you the science. You’d never understand it.)” I did, however, come up with some hits.
Recall that the presence of liver glycogen inhibits ketosis, so after a carb load we want to get rid of that nasty hepato-starch as quickly as possible… ideally without soaking up too much intramuscular glycogen, which we’ll want to have around next time we lift. From this remarkably non-histrionic article, we discover that alcohol inhibits gluconeogenesis in the liver. It does this by inhibiting the conversion of lactate to pyruvate; it’s been a while since I’ve done any skill-grinding on ketogenic diet physiology but this doesn’t strike me as directly relevant; it removes a pathway for the liver to generate glucose, but if the liver’s stocked up on glycogen that pathway would be too much effort.
The article also indicates that alcoholic ketoacidosis usually happens after “starvation” (that is, a day or three of fasting), and while we’re going to take advantage of the acute fasting response and its increase in growth hormone and catecholamines that’s going to happen after we drop a few fingers of whiskey. We would like to lift, then eat, then drink, then fast for sixteen-odd hours; and we’d prefer to spend as much of the fast as possible in ketosis. Drinking at the end of the fast, while pleasant, isn’t the operative variable.
This “helpful” little thing reinforces the idea that alcoholic ketoacidosis results from inhibited gluconeogenesis after glycogen depletion. Glycogen depletion’s what we’re after, so about the best we can hope for from inhibited gluconeogenesis is that a drink or three will shut down some of the complementary glucose-releasing processes in the liver and put greater demand on hepatic glycogen stores.
(This blog post has been interrupted by the Patriots remembering that there’s a football game going on in the second half.)
However, all is not lost. This abomination, aside from the quality of the reporting giving me cancer, suggests that… well, I’ll let the paper title speak for itself: “Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via NO and vagally mediated mechanisms”. It sure looks like acute alcohol consumption can trigger insulin release, leading to hypoglycemia, which would presumably lead to hepatic glycogen release into blood glucose. Which, y’all will recall, is what we want.
If it’s relevant, which is a big “if”, this’d play right into the Carb Backloading strategy of a big but short-lived insulin spike right before bedtime, disposing of any blood glucose left over from the carb load (or, presumably, liver glycogen if you don’t carb-load the night before a non-lifting day) and setting up a prompt growth hormone spike once you get to sleep. On the other hand, recall that my research methodology is “dick around on Google Scholar until something interesting happens on Sunday Night Football”, so take this with a pillar of salt.
Blunt Object 