On a ketogenic diet the muscles produce much less lactate than on a mixed diet.
Lactic acid is a product of carb metabolism. Ketones are the result of diminished carbs![/quote]
Those are completely irrelevant sources. The first one is just a blog response without any source backing it up. The pubmed reference is related to tumors and cancer having nothing to do with exercise induced lactic acid production.
On a ketogenic diet the muscles produce much less lactate than on a mixed diet.
Lactic acid is a product of carb metabolism. Ketones are the result of diminished carbs![/quote]
Those are completely irrelevant sources. The first one is just a blog response without any source backing it up. The pubmed reference is related to tumors and cancer having nothing to do with exercise induced lactic acid production.[/quote]
Don’t get me wrong I believe there could be something here, I just think at this point it would be presumptuous to say if and how much lactic acid production was reduced during starvation. It requires substantiating the mechanisms which lactic acid is created (it appears there are multiple) as well as determining the mechanism for muscular fatigue if that is the case. Lactic acid buildup is one of the primary mechanisms of fatigue so if nothing else caused muscular fatigue endurance would improve in starvation which doesn’t seem right.
On a ketogenic diet the muscles produce much less lactate than on a mixed diet.
Lactic acid is a product of carb metabolism. Ketones are the result of diminished carbs![/quote]
Those are completely irrelevant sources. The first one is just a blog response without any source backing it up. The pubmed reference is related to tumors and cancer having nothing to do with exercise induced lactic acid production.[/quote]
Don’t get me wrong I believe there could be something here, I just think at this point it would be presumptuous to say if and how much lactic acid production was reduced during starvation. It requires substantiating the mechanisms which lactic acid is created (it appears there are multiple) as well as determining the mechanism for muscular fatigue if that is the case. Lactic acid buildup is one of the primary mechanisms of fatigue so if nothing else caused muscular fatigue endurance would improve in starvation which doesn’t seem right.
[/quote]
There is only one mechanism by which lactic acid is created-from sugar. No sugar=no Hla.
It causes fatigue ultimately by slowing down the production of energy from carbs! If you don’t have carbs to make Hla then you are going to already have muscular fatigue.
On a ketogenic diet the muscles produce much less lactate than on a mixed diet.
Lactic acid is a product of carb metabolism. Ketones are the result of diminished carbs![/quote]
Those are completely irrelevant sources. The first one is just a blog response without any source backing it up. The pubmed reference is related to tumors and cancer having nothing to do with exercise induced lactic acid production.[/quote]
The second one does. A ketogenic diet is used theraputically to lower lactic acid level, because on a ketogentic diet you don’t have glycolysis to make lactic acid.
[quote]mertdawg wrote:
Your body will use the carbs to replenish glycogen, and then turn the rest into fatty acids. For the most part, combining fat and carbs together will tend to make the carbs act like more fat anyway, except up to the level that the brain is going to use in a short period of time 2-3 hours, after. [/quote]
De novo lipgenesis is not a major factor in humans. With the exception of excess quantities (i.e., chronic intake above TEE), your body will store what it can and then utilize the rest as the preferential energy substrate; in effect, CHO oxidation will rise to match CHO intake at the expense of FA metabolism.
[quote]mertdawg wrote:
The second one does. A ketogenic diet is used theraputically to lower lactic acid level, because on a ketogentic diet you don’t have glycolysis to make lactic acid.[/quote]
But, the cited study really only suggests that lactate was reduced due to preferential utilization by HNSCC tumor cells, not because of reduced glucose availability (glucose and pyruvate levels were observed to have risen within the cancerous tissue).
[quote]mertdawg wrote:
The second one does. A ketogenic diet is used theraputically to lower lactic acid level, because on a ketogentic diet you don’t have glycolysis to make lactic acid.[/quote]
But, the cited study really only suggests that lactate was reduced due to preferential utilization by HNSCC tumor cells, not because of reduced glucose availability (glucose and pyruvate levels were observed to have risen within the cancerous tissue).[/quote]
So tell me this, is there a source of lactate or pyruvate other than through the process of glycolysis? My contention is that it is not accurate to say that lactate is an ALTERNATIVE energy source in the absence of glycogen, but that it is a way to get more energy from glycolysis.
[quote]mertdawg wrote:
Your body will use the carbs to replenish glycogen, and then turn the rest into fatty acids. For the most part, combining fat and carbs together will tend to make the carbs act like more fat anyway, except up to the level that the brain is going to use in a short period of time 2-3 hours, after. [/quote]
De novo lipgenesis is not a major factor in humans. With the exception of excess quantities (i.e., chronic intake above TEE), your body will store what it can and then utilize the rest as the preferential energy substrate; in effect, CHO oxidation will rise to match CHO intake at the expense of FA metabolism.[/quote]
So you can show me a gas exchange study that shows that someone on a zero fat diet is burning 100% carbs/0% fat at rest? Anyway, yes the primary effect of carbs is to greatly reduce fatty acid mobilization and use for energy.
Going below 10% carbs upregulated de novo lipogenesis. So does a few days of excessive carbs. But insulin sensitivity starts to drop with carbs at about 30% of daily needs. On a 2500 cal maintenence diet the highest insulin sensitivity occurs at around 120-180 grams of carbs a day.
Obviously if you only take in as many carbs as you use efficiently in the day, they won’t turn into fat, but that level is basically the level that the brain uses, plus as much extra room is available in the liver and muscle to store glycogen. If Glycogen is topped off, and you eat carbs you either will have damagingly high blood sugar, or store sugars as fat, in adipose and the liver.
[quote]mertdawg wrote:
So you can show me a gas exchange study that shows that someone on a zero fat diet is burning 100% carbs/0% fat at rest? Anyway, yes the primary effect of carbs is to greatly reduce fatty acid mobilization and use for energy.[/quote]
Quit being silly – my response was directly quoting your assertions that 1) all excess CHO goes to fat once glycogen is topped off and 2) that F+C makes carbs “act like fat.”
[quote]mertdawg wrote:
Going below 10% carbs upregulated de novo lipogenesis. So does a few days of excessive carbs. But insulin sensitivity starts to drop with carbs at about 30% of daily needs. On a 2500 cal maintenence diet the highest insulin sensitivity occurs at around 120-180 grams of carbs a day.[/quote]
I’d be interested in hearing your definition of what exactly that is and to also see your studies on insulin sensitivity and CHO intake… keeping in mind that I will actually read them and, therefore, hope for them to be more relevant than your tumor abstract.
“Excess” CHO in this context should only be labeled as such when they surpass daily TEE.
[quote]mertdawg wrote:
Obviously if you only take in as many carbs as you use efficiently in the day, they won’t turn into fat, but that level is basically the level that the brain uses, plus as much extra room is available in the liver and muscle to store glycogen.[/quote]
Are you under the impression that the only dietary CHO used “efficiently” (i.e., not turned to fat) are those burned by the brain or used to top off glycogen?
[quote]mertdawg wrote:
If Glycogen is topped off, and you eat carbs you either will have damagingly high blood sugar, or store sugars as fat, in adipose and the liver.[/quote]
Or, perhaps, have a directly available energy substrate to work with.
Synthesis of fat in response to alterations in diet: insights from new stable isotope methodologies.
"The somewhat surprising finding that DNL appears not to be a quantitatively major pathway even under conditions of surplus carbohydrate energy intake, at least in normal adults on typical Western diets, is discussed in depth."
De novo lipogenesis in humans: metabolic and regulatory aspects.
“Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE).”
Carbohydrate metabolism and de novo lipogenesis in human obesity.
“Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose…during this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively.”
Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man.
“The data imply that…fat synthesis from CHO will not exceed fat oxidation after one high-carbohydrate meal, even if it is uncommonly large. When a single high-carbohydrate meal is consumed, dietary CHO merely has the effect of reducing the rate of fat oxidation.”
REGULATION OF HEPATIC DE NOVO LIPOGENESIS IN HUMANS
“In terms of the whole-body energy economy, however, the absolute rate of DNL was once again relatively insignificant, representing only 3.3 +/- 0.8g of fat synthesized per day, or 9.3 +/- 2.3g of CHO converted to fat, even on the diet with 50% surplus CHO. We concluded that the addition of surplus CHO on the order of 1500 kcal/day to a mixed diet did not induce substantial flux through hepatic DNL, at least when given for five days.”
First off, I meant that combining carbs with fats makes the net effect on hormones, (primarily insulin), more like that of fat because the insulin spike is slowed and diminished. You don’t get as fast a rate of carbs put into muscles and so you don’t get any degree of temporary supercompensation. If you take in 75 grams of straight carbs, your muscle and liver will slightly overfill on glycogen temporarily. That is a major cause of the anabolic effect of carbs. Combine them with fat, and they don’t get loaded fast enough to have this effect. My mis-statement was that carbs get turned into fatty acids, not that the effect of combining carbs and fat diminishes the hormonal factors that make carbs unique. But the statement is still fundamentally true. IF all of your glycogen is topped off, then the carbs have to go somewhere.
They are either going to be put into glycogen, or they will stay in the blood as blood sugar, and that’s why diabetics may have to use their muscles to bring down high blood sugar. But the excess, even short term, has to go somewhere. No room in glycogen. So it will stay as blood sugar waiting to get used, or your body will turn it into fat to protect you from the harms of high blood sugar. That leads to fatty liver disease.
Second, I posted a couple of articles that I grabbed before running out the door, and I wasn’t too careful. This was because the argument he was making was that lactic acid becomes an energy source when glycolysis is low. That is, to my knowledge, not consistent with physiology. How does lactate become an energy source in the absence of glycolysis? It is a product of glycolysis. If glycolysis is low then lactic acid production is low. Though I will have to check to see if ketones may yield lactic acid.
So I am not trying to be argumentative here. I wrote some statements that overgeneralized because of haste.
But here is a summary of the points I am interested in, or want to propose:
If you are not eating peri-workout, then eating pure carbs sans fat, say 100 grams will produce a hormonal effect that will tend to push to overfill glycogen in muscle and liver, or at least “top” it off. If you eat fat, it will tend to raise triglycerides, provide the liver and some other organs with fatty acids for synthesizing fatty acids, and fatty molecules that your cells need, shuttle them to cells, perhaps load intramuscular fat stores, and then adipose, load MCTs into cells for energy, upregulate mitochondria for beta oxidation. If you eat some carbs with some fat, you get generally less of the “carb” response, a generally mild glycogen rebuilding in the muscles, more in the liver, decrease in mobilization of fatty acids from adipose so you can burn up the blood sugar, and if the blood sugar, and also liver sugar (ie fructose) is HIGH the body will start to make some into fatty acids, ie fatty liver, but this is a very small percent, though it adds up over time.
At rest, and up to well beyond BMR rates, no matter what you eat, your MUSCLES will use mostly fatty acids. I have tested people with gas exchange who ate less thatn 10% carbs, and they still were burning 90% fat at rest. So how does that happen? I am asking for speculation or knowledge here. Granted that explains why long distance runners end up with 6% fat. They burn fat while eating largely carbs. That doesn’t mean that carbs become fat though, but when a runner burns 50% fat and 50% carbs over the course of a day where they run a marathon, how do they maintain 6% bodyfat? (it should trickle away to nothing).
Lactate comes from glycolysis. If you use more fatty acids, or use them better, you get less lactic acid. There is no source of lactate except glycolysis. Changes in ability to use fat or carbs CHANGE over time based on diet, so the carb/fat question is not straightforward. It depends on how you are set up and what you have been doing.
So an interesting question to me is what happens when somebody eats a high carb maintenence diet, say 70% carbs, 15 and 15? Do they have almost no synthesis of fat? I think it becomes MUCH more important on such a diet to eat carbs in small doses, and I think that 70% carbs, say 450 grams a day (not counting training) is going to need to be eaten in at least 6 doses throughout the day to prevent regular spike of high blood sugar, and I think that regular spikes of high blood sugar are going to be the trigger for lipogenesis, fatty liver and adipose from carbs. Let’s say you eat 150 grams 3x a day, which is basically what the government recommends on a 2500 cal diet. OK if you eat more resistant carbs you will get a slower trickle for a few hours. But what does the body do with regard to substrates? Are we saying that it starts using 70% carbs for basic sitting around needs? I have never seen a resting gas exchange that shows more carbs burned than fat.
[quote]Gettnitdone wrote:
We know that not only do fats lower the glycemic index of carbs (therefore reducing insulin secretion) but they are also digested slower than carbs.[/quote]
As far as I know fats NEVER reduce insulin levels, i.e., insulin secretion is monotonically increasing in all three macros.
However, adding fats will indeed tame blood sugar levels.
[quote]Gettnitdone wrote:
We know that not only do fats lower the glycemic index of carbs (therefore reducing insulin secretion) but they are also digested slower than carbs.[/quote]
As far as I know fats NEVER reduce insulin levels, i.e., insulin secretion is monotonically increasing in all three macros.
However, adding fats will indeed tame blood sugar levels.
[/quote]
I think adding fat to carbs will greatly slow the rate of carb entry into the bloodstream which will stabilize blood sugar. So its not wrong to say that it decreases insulin LEVELs at a given point in time. It spreads it out more. I would say that fat buffers insulin levels, and it has almost no independent effect on insulin. Plus since insulin becomes less efficient at higher blood sugar levels, buffering blood sugar spikes will reduce total insulin secretion.
[quote]Gettnitdone wrote:
We know that not only do fats lower the glycemic index of carbs (therefore reducing insulin secretion) but they are also digested slower than carbs.[/quote]
As far as I know fats NEVER reduce insulin levels, i.e., insulin secretion is monotonically increasing in all three macros.
However, adding fats will indeed tame blood sugar levels.
[/quote]
I think adding fat to carbs will greatly slow the rate of carb entry into the bloodstream which will stabilize blood sugar. So its not wrong to say that it decreases insulin LEVELs at a given point in time. It spreads it out more. I would say that fat buffers insulin levels, and it has almost no independent effect on insulin. Plus since insulin becomes less efficient at higher blood sugar levels, buffering blood sugar spikes will reduce total insulin secretion.[/quote]
Yes, except the final part - total insulin secretion for a meal doesn’t seem to be reduced.
Yes, except the final part - total insulin secretion for a meal doesn’t seem to be reduced.
(Nice thread btw)[/quote]
OK, OK but still people who tend to combine fat with carbs will tend to maintain higher insulin sensitivity and so over a period of months and years they might have less insulin release from the same standardized meal. ???
Yes, except the final part - total insulin secretion for a meal doesn’t seem to be reduced.
(Nice thread btw)[/quote]
OK, OK but still people who tend to combine fat with carbs will tend to maintain higher insulin sensitivity and so over a period of months and years they might have less insulin release from the same standardized meal. ???[/quote]
Fats lower insulin sensitivy. FFAs in the blood lower insulin sensitivy
Synthesis of fat in response to alterations in diet: insights from new stable isotope methodologies.
"The somewhat surprising finding that DNL appears not to be a quantitatively major pathway even under conditions of surplus carbohydrate energy intake, at least in normal adults on typical Western diets, is discussed in depth."
De novo lipogenesis in humans: metabolic and regulatory aspects.
“Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE).”
Carbohydrate metabolism and de novo lipogenesis in human obesity.
“Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose…during this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively.”
Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man.
“The data imply that…fat synthesis from CHO will not exceed fat oxidation after one high-carbohydrate meal, even if it is uncommonly large. When a single high-carbohydrate meal is consumed, dietary CHO merely has the effect of reducing the rate of fat oxidation.”
REGULATION OF HEPATIC DE NOVO LIPOGENESIS IN HUMANS
“In terms of the whole-body energy economy, however, the absolute rate of DNL was once again relatively insignificant, representing only 3.3 +/- 0.8g of fat synthesized per day, or 9.3 +/- 2.3g of CHO converted to fat, even on the diet with 50% surplus CHO. We concluded that the addition of surplus CHO on the order of 1500 kcal/day to a mixed diet did not induce substantial flux through hepatic DNL, at least when given for five days.”[/quote]
You’re fun I like you. You need to teach me how to search primary lit. I almost died citing shit for antibiotic dosing
Yes, except the final part - total insulin secretion for a meal doesn’t seem to be reduced.
(Nice thread btw)[/quote]
OK, OK but still people who tend to combine fat with carbs will tend to maintain higher insulin sensitivity and so over a period of months and years they might have less insulin release from the same standardized meal. ???[/quote]
Fats lower insulin sensitivy. FFAs in the blood lower insulin sensitivy [/quote]
That is important. It looks to me like insulin resistance from fats is acute. Cells reduce glycogen synthesis and glucose oxidation and sensitivity of the cells to insulin drops WHILE the fatty acids are high. This is not the same thing as carb induced LONG TERM insulin resistance, (the cells becoming less receptive to insulin due to, well, receptor down regulation that is continuous, rather than acute.
So the fatty acids are making the cells less sensitive while the FFA’s are high, but they are not altering the cells basic insulin sensitivity that would persist in their absence.
Any evidence that high FFAs cause chronic insulin insensitivity, (beyond the actual period of high FFAs)?
Also the main issue is that fats slow down the entry of carbs into the bloodstream which will diminish the peak blood sugar, which will keep sensitivity higher in the long run (again chronic or lasting changes versus acute).
though I have never had a full and satisfactory explanation as to the difference between the “insulin response” to feeding and insulin resistance. FAts do not raise blood sugar, and so they don’t elicit a strong insulin response from the pancreas.
I have a question that somewhat relates to all this:
So Mert, for instance I’ve seen you recommend say 180-200g CHO on days when someone exercises with primarily heavy weights and low reps (since that isn’t burning much glycogen) and slightly higher CHO recommendations on days when someone goes with higher reps (or sprints) and taps into glycogen. Are those recommendations NET carbs, or total carbs? So for instance with the 180-200 recommendation, how would getting 35g of fiber per day fit into that; would you bump the recommendation up to 215-235 in that case?