If Lipolysis Produces So Much ATP, Why Is It Bad?

bodacious

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This topic seems to be a real blind spot in my understanding of metabolism.

Until now, I thought that the reason oxidation of glucose was the optimal, because it yielded the most ATP. But I'm not sure if that's accurate.

Why is lipolysis so bad? Or rather, why is restoring oxidative metabolism preferable to lipolysis?

From what I've read, lipolysis seems to produce a lot of ATP, at least in terms of molecule count

Glycolysis (1 glocose molecule) = 2 ATP
Full oxidative phosphorylation (1 glocose molecule) = 30-38 ATP
Lipolysis (1 fat molecule) = 120 ATP

Is this total number offset by mass? Or is there another reason that oxidative metabolism is superior (e.g. production of CO2)?
 

Brian

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I'm not sure I fully grasp it, but my understanding is that all of these pathways are present in a healthy person with a mixed diet, except that glycolysis will be substituted for more oxidative metabolism.

While oxidative phosporylation produces less ATP it does it faster and also produces more heat and CO2, also at a faster rate.

Lipolysis isn't bad. It's the preferred energy production for muscles at rest and in a healthy person their muscles should be utilizing it effectively.

Lipolysis has some potential downsides when it relies on stress hormones to liberate stored fatty acids and circulate them as major fuel for the whole body, instead of mostly just the muscles.
 

nomoreketones

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Here is my oversimplified understanding:

Look at the wikipedia article: Lipolysis - Wikipedia, the free encyclopedia
The article says, "The following hormones induce lipolysis: epinephrine, norepinephrine, ghrelin, growth hormone, testosterone, and cortisol." Epinephrine, norepinephrine, growth hormone, and cortisol are stress hormones. The whole Ray Peat idea is to keep stress hormones low. Therefore it is better to use oxidative metabolism and get your 30-38 ATP from glucose.

Keep in mind that you are always burning fat and glucose at all times with low stress hormones. But if your body has plenty of glycogen and therefore is utilizing glucose as your primary fuel then your body will not need to pump out stress hormones to free up energy and engage in more fat burning than usual. But if you are glucose deficient then you will end up with higher levels of stress hormones in your blood.
 
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bodacious

bodacious

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So the argument against VLC dieting then is more the stress of having low blood glucose, rather than relying on lipolysis as the main source of energy?
 

nomoreketones

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So the argument against VLC dieting then is more the stress of having low blood glucose, rather than relying on lipolysis as the main source of energy?

That is part of the reasoning. Another reason is the Randle Cycle but I'm not exactly sure how that fits into the reasoning - Randle cycle - Wikipedia, the free encyclopedia. It would be cool if someone chimes in and explains why it is bad if fat beats out glucose in the Randle Cycle.
 

Koveras

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I think it's important first to distinguish lipolysis and fat oxidation. They are related processes, but separate, and each have their own considerations.

Lipolysis is the breakdown of stored fat in the body into its usable form.

Fat oxidation is the burning of fat for energy.

Lipolysis is associated with the stress hormones, which mobilize fat stores when glucose/energy is low, but are associated with other deleterious effects as well.

Fat oxidation in general is less desirable than carbohydrate oxidation, because less CO2 is produced, and CO2 has a variety of beneficial effects (and low CO2 some negative ones).

Since fat competes with carbohydrates via the randle cycle, elevated fat can have negative implications whether it is exogenous (from food), or doubly so when endogenous through lipolysis.

Chris Masterjohn discusses this briefly in Danny Roddy's video here



Danny also talks about ketosis/lipolysis here

 
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bodacious

bodacious

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I think it's important first to distinguish lipolysis and fat oxidation. They are related processes, but separate, and each have their own considerations.

Lipolysis is the breakdown of stored fat in the body into its usable form.

Fat oxidation is the burning of fat for energy.

Lipolysis is associated with the stress hormones, which mobilize fat stores when glucose/energy is low, but are associated with other deleterious effects as well.

Fat oxidation in general is less desirable than carbohydrate oxidation, because less CO2 is produced, and CO2 has a variety of beneficial effects (and low CO2 some negative ones).

Since fat competes with carbohydrates via the randle cycle, elevated fat can have negative implications whether it is exogenous (from food), or doubly so when endogenous through lipolysis.

Thank you, those links were very helpful.

So ultimately it is the CO2 that's the missing factor in the mainstream view?
 

CoolTweetPete

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Thank you, those links were very helpful.

So ultimately it is the CO2 that's the missing factor in the mainstream view?

That is my general understanding. Haidut has said that a very accurate measurement of metabolic rate is CO2 via Capnometer.
 

jyb

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Fat oxidation in general is less desirable than carbohydrate oxidation, because less CO2 is produced, and CO2 has a variety of beneficial effects (and low CO2 some negative ones).

Per ATP, I read that less CO2 is produced on fats...but then per O2, I read that more APT is produced on fats. So if you breath at the same rate while consuming the same amount of calories from carbs and from fats, you generate more ATP from fat. (Assuming you are using all carbs oxidatively...) So is it a trade-off or am I missing something? I'm just talking about theory here, not what happens in practice when you want to predict how much will be generated from eating this or that.
 
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Koveras

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Per ATP, I read that less CO2 is produced on fats...but then per O2, I read that more APT is produced on fats. So if you breath at the same rate while consuming the same amount of calories from carbs and from fats, you generate more ATP from fat. (Assuming you are using all carbs oxidatively...) So is it a trade-off or am I missing something? I'm just talking about theory here, not what happens in practice when you want to predict how much will be generated from eating this or that.

6 molecules of O2 are required to oxidize 1 molecule of carbohydrate, 38 ATP produced, ~6.3 ATP per O2,

23 molecules of O2 are required to oxidize 1 molecule of fatty acid, 129 ATP produced, ~5.6 ATP per O2

So oxidizing fat both requires more oxygen and produces less CO2 per O2 (and per O2 as you mentioned the ATP is less or similar, which I believe may change slightly depending on the length of the fatty acid).

Technically you produce more ATP per molecule of fat oxidized (ie 9 calories per gram vs 4 calories per gram for carbohydrate) - but keep in mind the amount of fuel you oxidize / ATP you produce is based on your metabolic rate and needs, and not on what type of fuel you are oxidizing.

So if your metabolic rate is 2000 calories per day, you will oxidize enough fuel to generate 2000 calories worth of ATP, by whatever type of fuel, and any excess will be stored - thus there is no inherent advantage to using a denser fuel source.
 

Koveras

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I don't see the same results when I follow this Hyperlipid: Not really much about swimming underwater

Again, the amount of oxygen required and ATP produced from fat depends on the chain length.

The example I posted was from palmitic acid with 16 carbons - the "most common fatty acid (saturated) found in animals, plants and microorganisms"

The example the author of the blog used was "a theoretical six carbon section of a chain of a fully saturated fatty acid". I'm not sure how much relevance a theoretical section of a chain has. Or how much caproic acid (C6) one typically consumes.

Also, the author seems to insinuate that there is a [5%] performance advantage to running on fat. I'm not sure if he just means oxidizing fat, or if he means literally running.

Many studies have shown fat oxidation to be fairly unimportant for elite performance in endurance exercise.

Not sure if your thoughts around increased ATP per O2 related to exercise performance?

Sports Med. 2015 Nov;45 Suppl 1:S5-12. doi: 10.1007/s40279-015-0400-1.
Carbohydrate Dependence During Prolonged, Intense Endurance Exercise.
Hawley JA1,2, Leckey JJ3.

A major goal of training to improve the performance of prolonged, continuous, endurance events lasting up to 3 h is to promote a range of physiological and metabolic adaptations that permit an athlete to work at both higher absolute and relative power outputs/speeds and delay the onset of fatigue (i.e., a decline in exercise intensity). To meet these goals, competitive endurance athletes undertake a prodigious volume of training, with a large proportion performed at intensities that are close to or faster than race pace and highly dependent on carbohydrate (CHO)-based fuels to sustain rates of muscle energy production [i.e., match rates of adenosine triphosphate (ATP) hydrolysis with rates of resynthesis]. Consequently, to sustain muscle energy reserves and meet the daily demands of training sessions, competitive athletes freely select CHO-rich diets. Despite renewed interest in high-fat, low-CHO diets for endurance sport, fat-rich diets do not improve training capacity or performance, but directly impair rates of muscle glycogenolysis and energy flux, limiting high-intensity ATP production. When highly trained athletes compete in endurance events lasting up to 3 h, CHO-, not fat-based fuels are the predominant fuel for the working muscles and CHO, not fat, availability becomes rate limiting for performance.

J Appl Physiol (1985). 2016 Jan 15;120(2)7-13. doi: 10.1152/japplphysiol.00855.2015. Epub 2015 Nov 19.
Altering fatty acid availability does not impair prolonged, continuous running to fatigue: evidence for carbohydrate dependence.
Leckey JJ1, Burke LM2, Morton JP3, Hawley JA4.

We determined the effect of suppressing lipolysis via administration of nicotinic acid (NA) on fuel substrate selection and half-marathon running capacity. In a single-blinded, Latin square design, 12 competitive runners completed four trials involving treadmill running until volitional fatigue at a pace based on 95% of personal best half-marathon time. Trials were completed in a fed or overnight fasted state: 1) carbohydrate (CHO) ingestion before (2 g CHO·kg(-1)·body mass(-1)) and during (44 g/h) [CFED]; 2) CFED plus NA ingestion [CFED-NA]; 3) fasted with placebo ingestion during [FAST]; and 4) FAST plus NA ingestion [FAST-NA]. There was no difference in running distance (CFED, 21.53 ± 1.07; CFED-NA, 21.29 ± 1.69; FAST, 20.60 ± 2.09; FAST-NA, 20.11 ± 1.71 km) or time to fatigue between the four trials. Concentrations of plasma free fatty acids (FFA) and glycerol were suppressed following NA ingestion irrespective of preexercise nutritional intake but were higher throughout exercise in FAST compared with all other trials (P < 0.05). Rates of whole-body CHO oxidation were unaffected by NA ingestion in the CFED and FAST trials, but were lower in the FAST trial compared with the CFED-NA trial (P < 0.05). CHO was the primary substrate for exercise in all conditions, contributing 83-91% to total energy expenditure with only a small contribution from fat-based fuels. Blunting the exercise-induced increase in FFA via NA ingestion did not impair intense running capacity lasting ∼85 min, nor did it alter patterns of substrate oxidation in competitive athletes. Although there was a small but obligatory use of fat-based fuels, the oxidation of CHO-based fuels predominates during half-marathon running.

Eur J Appl Physiol. 2016 Apr;116(4):781-90. doi: 10.1007/s00421-016-3333-y. Epub 2016 Feb 5.
Carbohydrate dependence during prolonged simulated cycling time trials.
Torrens SL1, Areta JL2, Parr EB1, Hawley JA3,4.

PURPOSE:
We determined the effect of suppressing lipolysis via administration of Nicotinic acid (NA) and pre-exercise feeding on rates of whole-body substrate utilisation and cycling time trial (TT) performance.
METHODS:
In a randomised, single-blind, crossover design, eight trained male cyclists/triathletes completed two series of TTs in which they performed a predetermined amount of work calculated to last ~60, 90 and 120 min. TTs were undertaken after a standardised breakfast (2 g kg(-1) BM of carbohydrate (CHO)) and ingestion of capsules containing either NA or placebo (PL).
RESULTS:
Plasma [free fatty acids] were suppressed with NA, but increased in the later stages of TT90 and TT120 with PL (p < 0.05). There was no treatment effect on time to complete TT60 (60.4 ± 4.1 vs. 59.3 ± 3.4 min) or TT90 (90.4 ± 9.1 vs. 89.5 ± 6.6 min) for NA and PL, respectively. However, TT120 was slower with NA (123.1 ± 5.7 vs. 120.1 ± 8.7 min, p < 0.001), which coincided with a decline in plasma [glucose] during the later stages of this ride (p < 0.05). For TTs of the same duration, the rates of whole-body CHO oxidation were unaffected by NA, but decreased with increasing TT time (p < 0.05). CHO was the predominant substrate for all TTs contributing between 83 and 94 % to total energy expenditure, although there was a small use of lipid-based fuels for all rides.
CONCLUSION:
(1) NA impaired cycling TT performance lasting 120 min, (2) cycling TTs lasting from 60 to 120 min are CHO dependent, and (3) there is an obligatory use of lipid-based fuels in TTs lasting 1-2 h.

Note - No carbs supplied during exercise in the study above

J Appl Physiol (1985). 2001 Jul;91(1):115-22.
Effects of fat adaptation and carbohydrate restoration on prolonged endurance exercise.
Carey AL1, Staudacher HM, Cummings NK, Stepto NK, Nikolopoulos V, Burke LM, Hawley JA.

We determined the effect of fat adaptation on metabolism and performance during 5 h of cycling in seven competitive athletes who consumed a standard carbohydrate (CHO) diet for 1 day and then either a high-CHO diet (11 g. kg(-1)x day(-1) CHO, 1 g x kg(-1) x day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.6 g x kg(-1) x day(-1) CHO, 4.6 g x kg(-1) x day(-1) fat; fat-adapt) for 6 days. On day 8, subjects consumed a high-CHO diet and rested. On day 9, subjects consumed a preexercise meal and then cycled for 4 h at 65% peak O(2) uptake, followed by a 1-h time trial (TT). Compared with baseline, 6 days of fat-adapt reduced respiratory exchange ratio (RER) with cycling at 65% peak O(2) uptake [0.78 +/- 0.01 (SE) vs. 0.85 +/- 0.02; P < 0.05]. However, RER was restored by 1 day of high-CHO diet, preexercise meal, and CHO ingestion (0.88 +/- 0.01; P < 0.05). RER was higher after HCHO than fat-adapt (0.85 +/- 0.01, 0.89 +/- 0.01, and 0.93 +/- 0.01 for days 2, 8, and 9, respectively; P < 0.05). Fat oxidation during the 4-h ride was greater (171 +/- 32 vs. 119 +/- 38 g; P < 0.05) and CHO oxidation lower (597 +/- 41 vs. 719 +/- 46 g; P < 0.05) after fat-adapt. Power output was 11% higher during the TT after fat-adapt than after HCHO (312 +/- 15 vs. 279 +/- 20 W; P = 0.11). In conclusion, compared with a high-CHO diet, fat oxidation during exercise increased after fat-adapt and remained elevated above baseline even after 1 day of a high-CHO diet and increased CHO availability. However, this study failed to detect a significant benefit of fat adaptation to performance of a 1-h TT undertaken after 4 h of cycling.

J Appl Physiol (1985). 2000 Dec;89(6):2413-21.
Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling.
Burke LM1, Angus DJ, Cox GR, Cummings NK, Febbraio MA, Gawthorn K, Hawley JA, Minehan M, Martin DT, Hargreaves M.

For 5 days, eight well-trained cyclists consumed a random order of a high-carbohydrate (CHO) diet (9.6 g. kg(-1). day(-1) CHO, 0.7 g. kg(-1). day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.4 g. kg(-1). day(-1) CHO, 4 g. kg(-1). day(-1) fat; Fat-adapt) while undertaking supervised training. On day 6, subjects ingested high CHO and rested before performance testing on day 7 [2 h cycling at 70% maximal O(2) consumption (SS) + 7 kJ/kg time trial (TT)]. With Fat-adapt, 5 days of high-fat diet reduced respiratory exchange ratio (RER) during cycling at 70% maximal O(2) consumption; this was partially restored by 1 day of high CHO [0.90 +/- 0.01 vs. 0.82 +/- 0.01 (P < 0.05) vs. 0.87 +/- 0.01 (P < 0.05), for day 1, day 6, and day 7, respectively]. Corresponding RER values on HCHO trial were [0. 91 +/- 0.01 vs. 0.88 +/- 0.01 (P < 0.05) vs. 0.93 +/- 0.01 (P < 0.05)]. During SS, estimated fat oxidation increased [94 +/- 6 vs. 61 +/- 5 g (P < 0.05)], whereas CHO oxidation decreased [271 +/- 16 vs. 342 +/- 14 g (P < 0.05)] for Fat-adapt compared with HCHO. Tracer-derived estimates of plasma glucose uptake revealed no differences between treatments, suggesting muscle glycogen sparing accounted for reduced CHO oxidation. Direct assessment of muscle glycogen utilization showed a similar order of sparing (260 +/- 26 vs. 360 +/- 43 mmol/kg dry wt; P = 0.06). TT performance was 30.73 +/- 1.12 vs. 34.17 +/- 2.48 min for Fat-adapt and HCHO (P = 0.21). These data show significant metabolic adaptations with a brief period of high-fat intake, which persist even after restoration of CHO availability. However, there was no evidence of a clear benefit of fat adaptation to cycling performance.

Sports Med. 1998 Apr;25(4):241-57.
Strategies to enhance fat utilisation during exercise.
Hawley JA1, Brouns F, Jeukendrup A.

Compared with the limited capacity of the human body to store carbohydrate (CHO), endogenous fat depots are large and represent a vast source of fuel for exercise. However, fatty acid (FA) oxidation is limited, especially during intense exercise, and CHO remains the major fuel for oxidative metabolism. In the search for strategies to improve athletic performance, recent interest has focused on several nutritional procedures which may theoretically promote FA oxidation, attenuate the rate of muscle glycogen depletion and improve exercise capacity. In some individuals the ingestion of caffeine improves endurance capacity, but L-carnitine supplementation has no effect on either rates of FA oxidation, muscle glycogen utilisation or performance. Likewise, the ingestion of small amounts of medium-chain triglyceride (MCT) has no major effect on either fat metabolism or exercise performance. On the other hand, in endurance-trained individuals, substrate utilisation during submaximal [60% of peak oxygen uptake (VO2peak)] exercise can be altered substantially by the ingestion of a high fat (60 to 70% of energy intake), low CHO (15 to 20% of energy intake) diet for 7 to 10 days. Adaptation to such a diet, however, does not appear to alter the rate of working muscle glycogen utilisation during prolonged, moderate intensity exercise, nor consistently improve performance. At present, there is insufficient scientific evidence to recommend that athletes either ingest fat, in the form of MCTs, during exercise, or "fat-adapt" in the weeks prior to a major endurance event to improve athletic performance.

Pflugers Arch. 1998 Jul;436(2):211-9.
Fuel metabolism during ultra-endurance exercise.
Rauch HG1, Hawley JA, Noakes TD, Dennis SC.

Cyclists either ingested 300 ml 100 g/l U-[14C] glucose solution every 30 min during 6 h rides at 55% of VO2max (n=6) or they consumed unlabelled glucose and were infused with U-[14C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9+/-0. 1 mM, 27+/-4 nM and 2.0+/-0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100+/-13 to 71+/-9 micromol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 micromol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with 14C lactate in the circulation.

Med Sci Sports Exerc. 2002 Jan;34(1):83-91.
Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability.
Burke LM1, Hawley JA, Angus DJ, Cox GR, Clark SA, Cummings NK, Desbrow B, Hargreaves M.

PURPOSE:
Five days of a high-fat diet produce metabolic adaptations that increase the rate of fat oxidation during prolonged exercise. We investigated whether enhanced rates of fat oxidation during submaximal exercise after 5 d of a high-fat diet would persist in the face of increased carbohydrate (CHO) availability before and during exercise.
METHODS:
Eight well-trained subjects consumed either a high-CHO (9.3 g x kg(-1) x d(-1) CHO, 1.1 g x kg(-1) x d(-1) fat; HCHO) or an isoenergetic high-fat diet (2.5 g x kg(-1) x d(-1) CHO, 4.3 g x kg(-1) x d(-1) fat; FAT-adapt) for 5 d followed by a high-CHO diet and rest on day 6. On day 7, performance testing (2 h steady-state (SS) cycling at 70% peak O(2) uptake [VO(2peak)] + time trial [TT]) of 7 kJ x kg(-1)) was undertaken after a CHO breakfast (CHO 2 g x kg(-1)) and intake of CHO during cycling (0.8 g x kg(-1) x h(-1)).
RESULTS:
FAT-adapt reduced respiratory exchange ratio (RER) values before and during cycling at 70% VO(2peak); RER was restored by 1 d CHO and CHO intake during cycling (0.90 +/- 0.01, 0.80 +/- 0.01, 0.91 +/- 0.01, for days 1, 6, and 7, respectively). RER values were higher with HCHO (0.90 +/- 0.01, 0.88 +/- 0.01 (HCHO > FAT-adapt, P < 0.05), 0.95 +/- 0.01 (HCHO > FAT-adapt, P < 0.05)). On day 7, fat oxidation remained elevated (73 +/- 4 g vs 45 +/- 3 g, P < 0.05), whereas CHO oxidation was reduced (354 +/- 11 g vs 419 +/- 13 g, P < 0.05) throughout SS in FAT-adapt versus HCHO. TT performance was similar for both trials (25.53 +/- 0.67 min vs 25.45 +/- 0.96 min, NS).
CONCLUSION:
Adaptations to a short-term high-fat diet persisted in the face of high CHO availability before and during exercise, but failed to confer a performance advantage during a TT lasting approximately 25 min undertaken after 2 h of submaximal cycling.

Med Sci Sports Exerc. 2002 Sep;34(9):1485-91.
Effect of increased fat availability on metabolism and exercise capacity.
Hawley JA1.

Several procedures have been utilized to elevate plasma free fatty acid (FFA) concentration and increase fatty acid (FA) delivery to skeletal muscle during exercise. These include fasting, caffeine ingestion, L-carnitine supplementation, ingestion of medium-chain and long-chain triglyceride (LCT) solutions, and intravenous infusion of intralipid emulsions. Studies in which both untrained and well-trained subjects have ingested LCT solutions or received an infusion of intralipid (in combination with an injection of heparin) before exercise have reported significant reductions in whole-body carbohydrate oxidation and decreased muscle glycogen utilization during both moderate and intense dynamic exercise lasting 15-60 min. The effects of increased FA provision on rates of muscle glucose uptake during exercise are, however, equivocal. Despite substantial muscle glycogen sparing (15-48% compared with control), exercise capacity is not systematically improved in the face of increased FA availability.

Med Sci Sports Exerc. 2002 Sep;34(9):1492-8.
Effects of short-term fat adaptation on metabolism and performance of prolonged exercise.
Burke LM1, Hawley JA.

The concept of manipulating an individuals habitual diet before an exercise bout in an attempt to modify patterns of fuel substrate utilization and enhance subsequent exercise capacity is not new. Modern studies have focused on nutritional and training strategies aimed to optimize endogenous carbohydrate (CHO) stores while simultaneously maximizing the capacity for fat oxidation during continuous, submaximal (60-70% of maximal O(2) uptake [(.)VO(2max)] exercise. Such "nutritional periodization" typically encompasses 5-6 d of a high-fat diet (60-70% E) followed by 1-2 d of high-CHO intake (70-80% E; CHO restoration). Despite the brevity of the adaptation period, ingestion of a high-fat diet by endurance-trained athletes results in substantially higher rates of fat oxidation and concomitant muscle glycogen sparing during submaximal exercise compared with an isoenergetic high-CHO diet. Higher rates of fat oxidation during exercise persist even under conditions in which CHO availability is increased, either by having athletes consume a high-CHO meal before exercise and/or ingest glucose solutions during exercise. Yet, despite marked changes in the patterns of fuel utilization that favor fat oxidation, fat-adaptation/CHO restoration strategies do not provide clear benefits to the performance of prolonged endurance exercise.
 

800mRepeats

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Thank you, Koveras - as a recovering former fat-adapted endurance athlete, that was an interesting little read.
 

jyb

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The example the author of the blog used was "a theoretical six carbon section of a chain of a fully saturated fatty acid". I'm not sure how much relevance a theoretical section of a chain has. Or how much caproic acid (C6) one typically consumes.

Also, the author seems to insinuate that there is a [5%] performance advantage to running on fat. I'm not sure if he just means oxidizing fat, or if he means literally running.

Many studies have shown fat oxidation to be fairly unimportant for elite performance in endurance exercise.

Not sure if your thoughts around increased ATP per O2 related to exercise performance?

Thanks for digging up studies, I appreciate it. I was only asking about the theory, not what happens in practice. And high athletes sport is whole can of worms when it comes to that. I think I would also use C16 rather than C6.
 

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