I'm on a "fat-burning" workout - what's happening to me?
 

Here's the question. How will dietary carbohydrate alter the metabolism of a well fed athlete performing steady-state exercise at 60% Max Hr, which is assumed to be 100% aerobic muscle fiber recruitment for purposes of this question. However, basal metabolic requirements still need to be accounted for.

Here's the control subject:For sake of simplicity, 30-year-old male, 170lbs, will expend 1200 cal during 3 hours of sub-maximal exercise while ingesting enough water. (test subject is hydrated as well)

Here's the test subject: Identical twin of control subject, 170lbs, will expend 1200 cals during exercise, but will ingest 200cals of a 50/50 fructose/sucrose blend at 1 hour 2 hour mark during the workout.

Obviously, one athlete has accumulated a 1200 cal deficit, and other has also expended 1200 cals but ingested 400 cals of simple sugars - therefore that athlete is at an 800 cal deficit.

Question 1)Is it possible to ascertain the difference of stored energy-substrate utilization between the two athletes as a result of 1200 cals or metabolic activity?

Question 2)Is it possible to identify the whether or not the ratio of energy substrate utilization involving fatty-acid oxidation and adipocyte mobilization is affected?

Essentially, we know that both athletes are down 800 and 1200 calories respectively. But what every single lame fat-head wants to know is - which athlete "burned the most fat".
We also know that eventually, homeostasis will restore any disturbance of balance of metabolites in the blood by oxidizing fat. So the guy who didn't eat carbs does eventually - "burn the most fat."

But my Richard Cranium question is:In this scenario, how much does carbohydrate ingestion during exercise contribute to energy expenditures and how much of the recent carbohydrate is actually replacing energy substrates that are already mobilized and ready for oxidation. I'm trying to understand how the body discriminates between adipocyte mobilization and recently metabolized [created] blood-born energy stores. (that is, the carbs before they turn into glycogen or non-"free" fat cells)


See if you can figure that out from reading this.
Here's a great link, previously supplied by an esteemed forum member:
http://web.indstate.edu/thcme/mwking...ml#alternative

Here's the gist of the link:

Regulation of Fatty Acid Metabolism

In order to understand how the synthesis and degradation of fats needs to be exquisitely regulated, one must consider the energy requirements of the organism as a whole. The blood is the carrier of triacylglycerols in the form of VLDLs and chylomicrons, fatty acids bound to albumin, amino acids, lactate, ketone bodies and glucose. The pancreas is the primary organ involved in sensing the organism's dietary and energetic states by monitoring glucose concentrations in the blood. Low blood glucose stimulates the secretion of glucagon, whereas, elevated blood glucose calls for the secretion of insulin.

The metabolism of fat is regulated by two distinct mechanisms. One is short-term regulation, which can come about through events such as substrate availability, allosteric effectors and/or enzyme modification. The other mechanism, long-term regulation, is achieved by alteration of the rate of enzyme synthesis and turn-over.

1) Fatty acid and amino acid catabolism produce NH3 which becomes urea. A urine sample will tell the tale. A blood sample every minute can be used to track NH3.

2) VO2:CO2 ratio

Of course, the person who drank 400kcal of sugar may have 'burned' 1200kcal of fat, then added 400kcal of fat from the sugar. Does that count as 'burning' 1200kcal of fat? This is hypothetical though. In reality I'm sure an elevated blood sugar will block fat catabolism, and if all 400 sugar kcals are ingested the first minute the blood sugar will skyrocket, the insulin level jump, and most of the sugar get stored in adipose tissue within the first half hour. Then the blood sugar will plummet, leading to a performance loss, making aerobic work difficult, and delaying the eventual fat store mobilization. If the sugar is consumed in continuous small frequent doses it will keep blood sugar from dropping, but still not get elevated. This is a good place to be since slightly lowered blood sugar is tied to hGH excretion in the absense of cortisol and other stress hormones. (Many other factors matter of course.) Too low of a blood sugar is tied to stress responses, many of which make exercise counterproductive.

Carbohydrates ingested during exercise are liver glycogen sparing but not muscle glycogen sparing. So at the end of the workout athlete 2 would have higher liver glycogen stores but similar muscle glycogen concentrations and substrate utilization ratios (Bosch et al 1994, Nicholas et al 1999) Energy substrate utilization ratios are dictated by both muscle glycogen concentration and fiber type recruitment patterns; and are essentially independent on liver and bloodstream carbohydrate levels.

This is why rampant carbohydrate ingestion does not make one immune to fatigue. Even with bypassing the digestive system (via IV) carbohydrate injection at the rate of 1g/minute (!!) does not prolong time to exhaustion when exercising at high intensity. Rates of 3g/min have produced increased performance, only because that rate is greater than the maximal rate the liver can release carb stores.

However, the controls central governor will detect the falling carbohydrate levels and will elicit much greater sensations of fatigue. In reality the energy depletion / delivery model of exercise performance and fatigue is bogus. If you biopsy an extremely tired athletes muscle, huge quantities of energy are still available, just the brain chooses not to activate the muscle to the point of harm. Electrical stimulation can prove it will still contract forcefully if commanded.

However, I realize this will be altered by the whatever concentration of solute.

That's exactly what I would guess.

But what I trying to describe, is to somehow "inventory" the entire body's status of energy substrates and fat stores before and after the test and deduce how and why the "ratio" changed.

According to your statement, both subjects metabolized nearly identical quantities of fat, but one subject finished with a higher a caloric value of liver glycogen. That is my understanding.

I just wanted to know how much, if any "spills" out of the liver as triglycerides or some other oxidative substrate [due to carb intro]that could in theory decrease fatty-acid mobilization. I do understand the possible consequences associated with glucose regulation and insulin response, but these guys are supposed be in good shape and this is a 3 hour "steady state" effort.

Recently, I answered a question on another message board and advised that the role of carbohydrate during "long sub-maximal runs" was to keep blood glucose levels stable while the muscles continue to use fat for energy. In other words, the carbs ingested, have no or little effect on training adaptations of muscle fiber to oxidize fats efficiently. But they could help someone who suffers from low blood sugar for whatever idiopathic reason. (and as previously mentioned possibly cause it too.....)

Well we do know that people with diets high in simple carbohydrates tend to suffer from elevated triglycerides. However, we don’t find that athletes with high triglycerides perform better or recover faster. So does the liver release more fat when carbohydrates are ingested during exercise, maybe. Do those fats increase any performance measure, probably not. The effect could just be a liver defense mechanism to prevent fatty liver when eating at rest; like when calories-in is greater than calories-out, dump fat into bloodstream. The fat can just stay in the blood while the liver plays catch-up, all while the adipose tissue tries to buffer these swings.

Ooooooh! Central Governor Theory! :)

If you are exercising would you not stimulate the sympathetic nervous system, and in turn the catecholamines would suppress insulin secretion, even though there is increased blood sugar. You also said that you are using fructose, which I believe is not digested as easily as some other simple sugars. In this case I would think that the diabetogenic hormones are partly suppressing the synthesis of glycogen, but the increased blood sugar is being used for energy thus the body is using glycogen at a slower rate than if there were less blood sugar.

The increased blood sugar may have the effect of slowing the release of the diabetogenics, but the catecholamines would still have to be present for the fact that the heart rate is increased and they are responsible for a good part of that. That being said there would probably be less catecholamines in circulation in the person consuming the CHO's, and as a result they would use less fat and less muscle glycogen because the muscles have access to more glucose and thus do not have to break down as much glycogen to supply the muscle with fuel. It is already being provided in a usable form and the presence of epinephrine will enhance the uptake of glucose into the muscle.

NICHOLAS, CERI W.; TSINTZAS, KOSTAS; BOOBIS, LESLIE; WILLIAMS, CLYDE (1999)
say that
"In summary, the ingestion of a 6.9% carbohydrate-electrolyte
solution providing 51 g CHO·h-1 during 90 min of intermittent
high-intensity shuttle running resulted in a 22% reduction in
the amount of muscle glycogen utilized, compared with drinking
a noncarbohydrate placebo. This may explain the improvement
in endurance capacity when soccer players ingested an identical carbohydrate-electrolyte solution immediately before and during
a similar exercise trial"


NICHOLAS, CERI W.; TSINTZAS, KOSTAS; BOOBIS, LESLIE; WILLIAMS, CLYDE (1999). Carbohydrate-electrolyte ingestion during intermittent high-intensity running. Medicine and Science in Sports and Exercise.

I think you meant 50/50 fructose/glucose blend, no? (sucrose = fructose + glucose, your formula as written would yield 75/25 fructose/glucose...?).



Anyway, the correct answer is: both subjects will post on BikeForums asking, "I'm working out a lot but I'm not losing any weight?!?!?!?arrrrgh!" and then 400 people will reply giving 450 different answers on what they should be doing instead. And at least one post will say "you must consume at least 250 cal/hr when riding!!!!1111one (or you will die)". Fact. Look it up.

Could the increase in triglycerides in the consumption of simple carbs be due to the insulin spike causing an increased absorption of glucose resulting in rebound hypoglycemia, which in turn leads the the release of diabetogenic hormones causing an increase in serum levels of triglycerides? As a result it may not be a defense mechanism to reduce the chance of liver morbidity but merely a response to low glucose levels.

Okay, everybody backup for a minute. The purpose of the discussion is to provoke unique perspectives but remain understanding of the limitations of any discussion using only the context of this "laymans" hypothesis.

First of all the reason I specified a mono/di-saccharide blend was to account for at least some metabolic "cost" of ingestion in the "problem". It wouldn't be realistic to specify pure glucose.

Secondly, my previous conclusions regarding carbs being used to replace liver glycogen have problems.

If you need to reread the "setup section" and remember that I had a line in the "testing" that says these athletes are "well fed". The reason I added that line was to presuppose that the athletes begin the exercise with fully topped-off liver/muscle glycogen stores.

The meaning of "topped off" was suppose to infer, that none of the ingested carbs could add directly to glycogen storage in the liver. Which brings me to the point that I don't even understand the mechanisms that limit continuous addition of glycogen to the liver.

If you can follow my "problem", what I am asking is: "What happens to the 400 cals of carbs if they are not able to be stored into liver glycogen?" I wanted to know if "fresh lipocytes" were entering the blood stream -- even as "older" fatty acids were being transported to muscle areas for oxidation?

The purpose of the discussion is to identify the difference in how pools of energy substrates shift differently between athletes ingesting carbs and those restricting carbs. For now, performance is not the issue. Also, I noted that some have posts, have ignored the setup data, and are referring to studies that are using exercise intensities that require primarily gylcogen.

This discussion is about completely aerobic, "all day" cycling activity, not a mix of intensities.

Who has the down and dirty about what "limits" glycogen storage in a given liver? Does size matter? Is it cell quality? Who knows how to predict the proportion of glucose/fatty acids needed to expend 1200 calories across 3 hours for 170lb 30-year-old male?

What's the "basal carb requirement" for 3 hours? Probably ~350-400? Does this mean any 3 hour, 1200 calorie ride can only burn 800-850 cals of actual fat, no matter what?

Most of the time, what happens in these discussions, the original context is lost. Please no shifting this time.

If you change the composition of the blood by adding CHO's would you not change the bodies response to the change in blood composition, in the form of hormones?

In this case you would increase the blood glucose level, this in turn would change the balance between insulin and the catecholamines. The nature of the catecholamines is to increase glucose uptake in the muscle thereby reducing the amount of blood sugar, and in turn less glycogen in the muscle is used. The presence of glucose will slightly reduce the release of catecholamines thus slowing glycogenolysis, and lipolysis.

This figure is good in that it further breaks down fat and carb usage into the muscle: plasma contribution ratio.

!!Comatoa$ted you raised some good food for thought.

I suspect that the 400 cals would be used to fuel the muscle thus sparing glycogen in the muscle. As soon as the liver received the chemical message, due to the increase in blood glucose, it would slow down lipolysis. Since there is a need at the time for glucose, the muscles will use it because it is available, thus sparing glycogen. If at the end of the test the people are resting and recovering and there is excess glucose in the blood it will be used towards glycogen stores thus avoiding hyperglycemia. Lipolysis at the time of the CHO digestion would probably provide some fuel, and if there was extra lipid monomers in the blood in excess they would probably be made into fats, or just circulate until an anabolic hormone started being released to build it into a fat.

That is an interesting chart. What happens if you raise the blood glucose how would that effect the rest of the numbers shown? Is there a way to manipulate it by changing blood sugar concentrations?

ding ding ding - we have a winner

Can you post the link to where this came from?

Essentially, this is exactly what I wanted to see. Something that could bring together the proportions of metabolites affected as intensity changes.

But what would really drive home - or illustrate? - the topic??? What I want to demonstrate, is how everyone's body composition is in a "dynamic state of flux" -- trying to catch up with energy demands and stow-away energy surpluses.

Some kind of time line slide show, depicting how exercise and eating affects the blood and organ tissues first and then goes on and on until "homeostatic" balancing hormones start either breaking a part fat cells or continue to fill them.

The two major areas on interest is how the blood is not only transporter of nutrients, but also a background "war zone" of competing chemical messengers trying to sort out what's best for the body overall.

And finally, some kind of simple charting of how after exercise, or after eating a big turkey dinner, it all settles down within 6 or 7 hours and you are left with --- YOU ARE WHAT YOU EAT, or YOU ARE WHAT YOU EXERCISE.

So what is the time frame, after the cessation of exercise, that these two guys eventually lose 800cal and 1200 cals of body fat? Assuming no additional activity after the 1200 cal work out, I'm supposing the body-fat would indeed be completely mobilized and metabolized in 3-5hour span, and the blood/plasma returned to pre-workout status.

Sorry, no idea. It was just on my hard disk; I have a habit of saving interesting images.

Ok I drew a little scribble to help cut off a few paragraphs. Your question relates to the kinetic control aspect of metabolic processes.

Can anybody provide the maximal rate at which each arrow can occur? Express in Cal/hour; this will tell the whole tale.

My moderately educated guess of the rate-determining step would be:

For the athlete who is eating large amounts of carbs and is exercising at high intensity, the rate of reaction arrow 1 is most likely limiting his recovery.

For the athlete attempting to burn off his gut by starving himself while exercising at very low intensity is ultimately limited by arrow 2. (Control)

For the athlete eating skewed macronutrient ratios (low-carb), liver function (arrows 3) will limit his recovery.

Can we control the rates and ratios?

Maybe by selection of:
-Low vs high glycemic index carbs?
-Type of fat consumed (chain length, degree of unsaturation)?
- Protein choice (amino acid profile and degree of hydrolysis)?
- Abuse insulin (Marco Pantani)?
- Caffeine (glycogen sparing)?

Discuss.

I was thinking more about trying to come up with some kind "demarcation" of how body composition has quite a time lag in responding to "pigging out" as well as fasting or exercise.

For instance, the necessity of "fasting for 12 hours" before drawing blood for a lipid panel. How does one go about explaining the nature of adipocytes, with respect to triglyceride and cholesterol levels?

For that matter, the nature and transport of medium chain fats and triglycerides to muscle tissue.

There's another new lame-o question just posted, the "empty-stomach" fat-burning workout......