Taking carbs immediately before, or while running

(Michael - When reality fails to meet expectations, the problem is not reality.) #30

From the study linked by @ctviggen above:

… Nevertheless, fatty acids are taken up during brain development, and it has been reported that fatty acid oxidation could contribute up to 20% of the total brain energy requirement.15, 16 In addition, fatty acid-binding proteins and carnitine have been found in the brain tissue,17 suggesting that fatty acid metabolism has a role in neurodevelopment, neurotransmission, and repair processes.18 Moreover, carnitine, widely known for its major role in transport of fatty acids across the inner mitochondrial membrane, is indeed essential for brain functioning.19…

Figure1 shows the two major steps in the route of fatty acid metabolism in neural cells. Long-chain fatty acids circulate in the nonesterified, albumin-bound form in the blood. After dissociation from albumin, in the first step, NEFA have to migrate across the BBB and, thereafter have to enter neural cells. NEFA become activated to acyl-CoA-derivatives in the cytosol of neural cells. In the activated form, fatty acids are either used for the esterification to membrane lipids or in the β -oxidation. The latter represents a plentiful source of reducing equivalents NADH and FADH2 inside the mitochondria. Oxidation of both types of reducing equivalents by the electron transport chain (ETC) generates the electrochemical proton gradient, the driving force for ATP synthesis.

As outlined in Figure 1, the reluctant oxidative utilization of fatty acids in the brain tissue raises three important questions: First, does the BBB limit the uptake of NEFA by the brain parenchyma and neural cells and therefore reduce the availability of fatty acids for metabolic consumption in the brain? This question will be discussed in the next chapter. The second question is whether fatty acid uptake would override oxidation. This imbalance results in the accumulation of fatty acids in the free and/or in their esterified forms in the cytosol. Thus, it could be that brain mitochondria are particularly vulnerable against high concentrations of NEFA and those of acylcarnitines and/or acyl-CoA-thioesters. This might explain that mitochondria from individual types of tissue differ considerably in their enzymatic equipment for the oxPhos machinery.26 The third question is, whether possibly further drawbacks exist. This is indicated by the fact that substantial fatty acid oxidation increases the risk of neural tissue to become hypoxic, which would not be compatible with rapid and sustained neuronal signaling. These latter issues are discussed in the last chapter and lead to a further clue to understand the low usage of fatty acids for brain energy, which has not been considered so far.

(Edith) #31

@ctviggen, thanks for posting that article. I think I may have heard Zach Bitter mention being a participant in that study.

From the discussion section of the paper:
“The most notable findings were that compared to HC athletes, the LC keto-adapted runners showed: (1) two-fold higher rates of peak fat oxidation during graded exercise, (2) greater capacity to oxidize fat at higher exercise intensities, (3) two-fold higher rates of fat oxidation during sustained submaximal running, and (4) no differences in pre-exercise muscle glycogen concentrations, the rate of glycogen utilization during exercise, and the rate of glycogen synthesis during recovery.”

I found this very interesting. I had read elsewhere that it takes longer for muscle glycogen to get replenished when following low carb, but their results showed otherwise. It also mentions that the low carb athletes used less muscle glycogen, but that makes sense. If they are burning more fat, they need less glycogen.

I have seen advice that states if one wants to exercise twice a day, it is good to eat carbs to get the muscle glycogen restored before the next workout. Maybe we just need to eat enough low carb food to replenish, it doesn’t necessarily need to be carbs.

All the test subjects had been low carb for some time and were fat adapted. I’m curious, @cooked, how long have you been eating keto?

(Bacon is a many-splendoured thing) #32

I have no idea how we would go about verifying that the brain can use fatty acids as well as ketones, given that the blood-brain barrier won’t let fatty acids pass through. I’m having a hard enough time as it is, without giving up some of my precious brain tissue to be studied under a microscope! :grin:

(Michael - When reality fails to meet expectations, the problem is not reality.) #33


(Bacon is a many-splendoured thing) #34

Two pieces of the puzzle to ponder: first, muscle glycogen cannot be shared, but liver glycogen can be. I have read somewhere that the product of gluconeogenesis is stored as liver glycogen, and then, when explosive power is needed, the liver glycogen gets turned back into glucose and released into the bloodstream for the muscles.

The second piece is that muscles much prefer fatty acids to ketone bodies, which are partially metabolised fatty acids.

So from this, I conclude that in a fat/keto-adapted athlete, the equation is Energy = muscle glycogen + liver glycogen + fatty acids. Phinney says that as far as endurance is concerned, running on mostly fatty acids makes an athlete bonk-proof. As far as explosive power is concerned, however, the anecdotal experience of forum members is that their endurance performance returned a lot sooner than their explosive power. And yet we know from the Volek study that by two years of keto-adaptation explosive power had returned in the athletes they studied.

I can’t seem to shake my idea about the difference between circulating ketones versus production and consumption. I guess you don’t find it at all satisfactory as an explanation. My understanding of the dawn phenomenon is that the body is preparing to make explosive effort possible in case of need (such as waking up to find a sabre-toothed tiger invading your cave). It also makes sense that serum glucose would rise during exercise, so as to be available for explosive performance as needed.

As far as cells that require glucose and that cannot use fatty acids or ketones are concerned, that would be primarily the erythrocytes (red blood corpuscles) and certain parts of brain neurons that are too narrow to contain mitochondria (this latter, according to Dr. Georgia Ede). I believe I have read that there are certain other cells that also cannot handle fatty acids or ketones, but no longer remember what cells those might be. And of course Prof. Bikman contests the notion that the brain needs any glucose at all, maintaining that it can get 100% of its energy from ketone bodies.

(Michael - When reality fails to meet expectations, the problem is not reality.) #35

The brain may very well make it’s own ketone supply and not rely on liver synthesized ketones at all or only slightly. Thus, it’s possible that low circulating ketones do not reflect the degree of ketone usage in the brain. This could explain why those of us on keto for several years and fat adapted can measure very low/no ketones, but still have a healthy, functioning brain. See my links in comment 33 above

I’ve decided to follow up on this possibility and post my findings here:

(Edith) #36

I just finished listening to this podcast where Zach Bitter talks a fair bit about what he eats. It seems workout intensity definitely comes into play where his use of carbs is concerned.

#37

Today I did 45 minutes on the bike again but with no sprints and I kept my heart rate around 120-125. This time my BG did not come down and was 100 mg/dl when I tested after my ride. So it may well be the case that the BG is only used in the “explosive” moments.

(GINA ) #38

I wore a CGM for a couple of weeks a while back and long endurance runs seemed to bring my BG down. I came back from 6 or 7 miles (which was long for me at the time) with BG in the high 60s, down from the 90s when I started the run.

For me, shorter, higher intensity workouts would leave me with higher BG. I think my body sensed it needed it, so released sugar from my liver and kept it up, where with the long, slower effort it drew my BG down without releasing a bunch.

I really don’t know exactly what was going on, but that makes some sense to me.

(Michael - When reality fails to meet expectations, the problem is not reality.) #39

Stop the presses!

The paper (unfortunately behind a paywall):

A discussion:

(David Cooke) #40

In my unhappy experience drinking a cold beer immediately after a hard run results in me feeling very ill. I have seen the same thing happen to others.
However I’m happy to know that a beer or two the night before a run is more or less OK.

(GINA ) #41

I am not a huge beer drinker, but if there is a post-race beer offered at the finish line I am drinking it, even if it is only 10:00 am.

I even took a small cup once from stranger set up at mile 12 of a half. :grinning: It was delicious.

(Butter Withaspoon) #42

At mile 12 and a half you take anything you can get! :laughing:

(Kenny Croxdale) #43

Hybrid Car Analogy

Your body is similar to a Hybrid Car in how it operates.

Electric Battery = Ketones

For long drives that that don’t require much power, the Electric Batter provides the fuel/energy.

Think of the Electricity in this case as being your Ketones.

Gas = Gliucose

When you need power, to let’s say pass another car, Gas is used.

Think of Gas in this case as being Glucose.

with that in mind, let’s look at…

The Three Energy Sysysems

  1. Phosphagen Energy System

This system run primarily off ATP, Andenosine Triphophate; rather than Glucose or Ketones.

Highly Intentive exericse that around 15 second or less; not longer than 30 seconds use ATP.

Thus, Keto Adapted and Standard American Diet (High Carbohydrate Diet) indifiduals perform equally as well in this Energy System.

ATP Muscle Restoration for the next set of an exercise occurs with Ketones and some Glucose, producing an increase in some blood sugar.

  1. Glycolytic Energy System

This involve fairly high intensive exercise that is over 30 seconds and less than 2 minutes.

Individuals in sport or who employ exericse in the Glycolytic Energy System, perform more effectively on a higher carbohydrate diet; this is a Glucose Dominate System.

  1. Oxidative Energy System’

This is one of the most researched areas, when it come to Keto Adapted individual.

Endurance Athletes and exercises last longer than 2 minutes plus, utilize more Ketones (body fat) in this Energy System.

As we know, the lower the intensity of the “Activity” the greater the percentage of Ketones used; with very little Glucose being used.

Sleeping Example

Sleeping is the lowest form of “Activity” (Inactivity) their is.

Thus, it burn the greatest percentage of body fat (Ketones) and utilized viturally no Glucose.

However, it doesn’t burn many calories; unless you are a hybernatiing bear.

“… Male bears may lose between 15% to 30% of their body weight during hibernation , while lactating females may lose up to 40%.” http://bearsmartdurango.org/black-bears/hibernation/#:~:text=Hibernating%20bears%20have%20the%20ability,may%20lose%20up%20to%2040%.
:
:Kenny Croxdale

(Bob M) #44

I’m not against this, just that I have cardiomyopathy (a type of heart failure). There’s a lot of evidence that implies the heart loves ketones in this situation. This implies it would behoove me to have high ketones…but I no longer get them unless I fast multiple days.

I can see that, over time, the difference between consumption and production become much closer. It’s just a little disconcerting for someone like me.

(Bob M) #45

This could be true. I only do what I would characterize as “high intensity” workouts. For instance, if I ride my bike, I ride it a short distance to hills and ride up and down them. If I do body weight training, it’s always to failure (if I’m doing pushups, I do them until I can’t do them anymore).

The only exception would be working on the house. But that might be intense exercise separated by intense exercise.

(Bacon is a many-splendoured thing) #46

Do you mean “high ketones” in the sense of abundant production, fairly closely matched by consumption, or in the sense of production that measurably outstrips consumption?

(Michael - When reality fails to meet expectations, the problem is not reality.) #47

@ctviggen @PaulL My major questions involve the brain and ketones. Like you, Bob, I measure very low ketones whenever I measure (4 1/2 years in ketosis). If a ‘brain on ketones is a healthy brain’ or at least healthier how does my brain get them? Is my brain even healthy? I don’t have any symptoms to indicate anything particularly wrong, so I presume it is. I have BG in the mid-low normal range and eat to remain consistently in ketosis. So how much energy does my brain derive from ketones and glucose? I don’t know. See my links here, which I linked above as well, that indicate the brain may, in fact, synthesize it’s own supply of ketones. If this is the case it could help explain why long-term keto/fat-adapted folks measure low ketones generally and still avoid the various degenerative diseases of the brain. If the brain makes its own that’s a huge amount the liver no longer has to produce. And I think would significantly reduce the amounts traversing the bloodstream at any given moment of measurement. Plus, for those of us in maintenance with relatively low BF, it would retain a consistent supply of ketones to the brain while ketogenesis in the liver might not be producing much simply because we’re not eating sufficient fat to overwhelm the acetylCoA pathway.

(Bacon is a many-splendoured thing) #48

If you are are keeping your carb intake low, then your liver is making either ketones or glucose to feed your brain. In a low-carb state, the insulin/glucagon ratio is low, thus favouring ketogenesis (gluconeogenesis also occurs but is pretty tightly regulated), so I’d say your brain is being fed mostly on ketone bodies.

Cahill demonstrated this in the 1960’s by subjecting his fasting subjects to a hyperinsulinaemic euglycaemic clamp, driving their serum glucose to levels low enough to cause hypoglycaemic coma or death, but the subjects were fine. (As Dr. Phinney remarks in a few of his lectures, “the people sweating and trembling were the ones in the white coats.” This was actually a highly unethical experiment, but it was illuminating, nevertheless.) Since the research subjects were well into the ketosis of fasting, this demonstrates that the brain is able to get a high percentage of its fuel (if not all) from ketone bodies. Unlike fatty acids and triglycerides, ketone bodies can readily pass the blood-brain barrier, or so I understand.

We regularly get forum members with CGM’s posting that their serum glucose has dropped to worrisome levels, yet they feel fine. We tell them not to worry about it, unless they start showing symptoms of hypoglycaemia.

(Bob M) #49

It’s a difficult question. I’m also concerned about my heart. Does it primarily use ketones? And if so, how since my ketones are so low?

As for a lot of this, there really aren’t studies on people who have been keto for a long time. I listened to someone who measured BHB in the Masai and the Hazda. The tests came back as 0.1mmol/l or so. Similar to us.

So, this has to be evolutionarily sound.

I would assume that the “substrates” transition after a while to ketones, free fatty acids, with less reliance on glucose. But how long that takes and why (and is it “bad”?) are all up in the air.

@PaulL For the ketones, most of the testing for heart failure and ketones is based on “higher” ketones. But most of them are animal models.

I have seen a lot of anecdotal evidence that keto works, but not many RCTs. Here’s one, but I don’t see any outcome:

But even if these happen, I’m sure the people being treated will have higher ketones, as I did at one time.

I have been thinking about doing a PKD to see what happens. Would ketones go up? If so, would I feel better? I just haven’t had time to do this.