# What are you really burning during exercise?

Warning - This will be a long technical post, but if you want to figure out how exercise intensity and fuel utilization (ration of Carbs to Fat burned) are related, I suggest taking the time to hear me out.

When reading John Berardi’s column about glycogen depletion, he talks about the ratio of fuels (C and F) being burnt as a function of exercise intensity. I want to present another point of view that one of my professors was working on until he unfortunately passed away from a heart attack a year ago. When exercising you consume oxygen (VO2 = oxygen consumption rate) and produce carbon dioxide (VCO2 = rate of carbon dioxide production). There is a ratio called the respiratory exchange ration (RER) which is used to determine the ration of C and F being used. The equation is as follows: RER = VCO2/VO2. There is also another ratio called the respiratory quotient (RQ) and it has the same equation: RQ = VCO2/VO2. You need to know that the RQ is what is going on at the cellular level and we cannot measure this. Thus, we have to use the RER as an estimate of the RQ, but this is measured at the mouth, not the cell. Why is this a problem? There are sources of CO2 that are not linked to aerobic metabolism (the primary other source is anaerobic CO2 production). In general an RER of 0.7 is considered to be 100% F consumption and 0% C consumption. A ratio of 1.0 is considered to be 100% C, 0% F. The generally accepted theory is that as the RER increases you burn more C and less F. Remember that I am only talking about aerobic metabolism now. When you do a VO2 max test though, you will often see RER values of 1.2 +. When the generally accepted theory is asked to explain this phenomenon, it says that you are just burning 100% C and no F if you are at 1.0 or over. That does not seem to sit well with me. Why? Because it ignores the fact that on top of aerobic metabolism, there is a SIGNIFICANT amount of anaerobic metabolism at high intensity exercise.

OK, what is my point. At rest, we tend to generally burn the ratio of foodstuffs that we consume. Eat a high fat diet, you will burn more fat. Eat a high C diet, you will burn more carbs. My professor made the assumption that this ratio of foodstuffs will be burned throughout aerobic exercise. We can safely assume that RER = RQ at rest because there is no significant anaerobic metabolism. When we start to do cardio, we increase our energy expenditure and must increase metabolism to keep up. If you look at a graded exercise test where you work your way from low intensity exercise to max exercise, the RER does not change significantly at low workloads. Why, there is very little anaerobic metabolism. But as the intensity increases more and more the RER increase close to and then past 1.0 at max. Does this mean that we are only burning carbohydrate at high intensity. I don’t think so and I’ll try to explain why.

Lets just say for simplicity that your resting VO2 is 1.0 L/min (I know that is high, but I’m shooting for easy calculations) and your max VO2 is 4.0 L/min. I will also say that resting VCO2 is 0.7 L/min and max VCO2 is 5.0 L/min. IF you do the calculations: resting RER = VCO2 (0.85 L/min)/VO2 (1.0 L/min) = 0.85 and max RER = 5.0/4.0 = 1.25. Pretty big change in the RER and remember that generally accepted theory says that you are burning 50%F, 50%C at rest and 100%C at max. I don’t think that we really shift this much. The reason is that there are 2 primary sources of CO2 – aerobic metabolism and the CO2 produced by buffering Lactic Acid with bicarbonate. Lactic acid is a product of anaerobic metabolism and the bicarbonate is secreted by the kidney to help control pH. The generally accepted theory ignores the anaerobic CO2 production and I think that this is a mistake.

So we need to assume 2 things: 1) the resting RER is constant for AEROBIC metabolism and 2) the RER is changing because we are adding CO2 from anaerobic pathways. At a resting VO2 of 1.0 L/min we burn about 5 calories (1 L O2 consumed = 5 calories burned) and at a 50/50 ratio, we burn 2.5 cals of F and 2.5 cals of C per minute at rest. At max, we burn 20 calories (4 L O2 * 5), but we also have significant anaerobic metabolism going on that is burning an extra 10 calories (for this to work, you have to assume that I have my subject in a direct calorimeter and I can measure all heat produced while also using indirect calorimetry to calculate aerobic metabolism). So with the 20 calories of aerobic metabolism, we are still 50/50 and burning 10 cals F and 10 cals C. The other 10 calories coming from anaerobic metabolism are all C because we do not use fat anaerobically. So at rest, we were burning 2.5 cals F and 2.5 cals P (50% F, 50%P). At max, we burned 10 cals F and 20 cals C (33%F, 67%C). So yes, we do burn more C when exercise intensity increases, but we do not stop buring F. Aerobic metabolism is never shut down, rather you add anaerobic metabolism on top of it. So at max, those 5L of CO2 produced per minute were not all from aerobic metabolism, but rather 3.4 L were coming from aerobic CO2 production and the other 1.6 L of CO2 production were coming from anaerobic CO2 production that comes from buffering lactic acid with bicarbonate.

Note of caution: This really only applies to shorter durations of cardiovascular activity (generally less than 1 hour), but what bodybuilder does more than 1 hr of continuous cardio. Also, I have really simplified an incredibly complex subject. Also, the calculations were just an example. The message is that you need to read studies that talk about the RER/RQ with a note of caution. I don’t think that fat metabolism is shut off at any exercise intensity and I hope that I have at least provided some evidence to support this. Finally, I must thank Dr. Paul Mole for opening my eyes to this theory and helping me to learn that everything you read in a journal is not necessarily the truth.

Great post; you really know your stuff. One question, though: I’ve always thought that the resting VO2 is 3.5 ml/kg/min (1 MET). Above, you assert that it is 1.0L per minute. In fact, your VO2 values throughout the post are a lot higher than I’m used to (I normally see ml and not L). Am I way out in left field? Is this a different measure altogether? Am I converting something wrong? In spite of my ignorance, I’m glad that you were able to expand the body of knowledge, and I’m even happier that you brought it to the forum. Hopefully, it will quell some of the anti-cardio sentiment around here.

From somewhere in the middle of the original post:

Lets just say for simplicity that your resting VO2 is 1.0 L/min (I know that is high, but I?m shooting for easy calculations)

Eric - you are right. In general RMR is usually about 1 MET = 3.5 ml/min/kg = ballpark 0.2-0.4 L/min depending on body weight. As far as whether you put terms in the relative (ml/min/kg) or absolute (L/min), it depends on the point you are trying to make. BTW, at my peak of cardiovascular conditioning, my VO2max was 57ml/min/kg or 4.6 L/min. I, in no way, am a very good endurance athlete and these were at a body weight of 176 lbs (I’m now about 205). The numbers that I used for my example were very reasonable at max, but also very high at rest. I only chose the 1 L/min value for easy calculations. As I’m now working in the real world, I desperately miss my teaching duties from Grad school, so the forum is my best outlet when I feel like ranting on a certain topic.

You are right in that many people take studies that cite RER values as gospel with regard to substate utilization. Even worse, many studies actually report RER values, but present them as RQ. Now, if you are measuring arterial/venous O2 and CO2, you are measuring RQ, but too often I have read a paper where the authors used a metabolic cart to determine substrate utilization and reported RQ. The value of RER as an absolute measure of substrate utilization is really limited, especially during exercise due to the dynamic changes that are happening with regard to metabolism. Even at rest though, it is not uncommon to measure RERs in the low 0.7s. Does this mean that the individual is oxidizing only fat, as the definition of an RER of 0.7 states, not likely. Conversely, if using an arm crank ergometer, it would be relatively simple for an individual to reach an RER of 1.0. Does this mean the individual is oxidizing only carbohydrates in their entire body? No. It is likely CHO is being oxidized at a high rate in the arms, bicarbonate is being blown off, but the legs may be oxidizing primarily fat. RER is just an estimation of whole body substrate flux. So, RER is really only of value for relative comparisons between similar treatments.

Please excuse any type of ignorance I may project here. This was a unbelievably interesting post. Anyways, I have a tendency to read articles like these and at the same time, try to translate them in “layman’s” terms. Y’know in case I have to expain it to someone who is not so familiar with such “stuff”. As I was reading this, one particular athlete came into mind that best incorporates both aerobic and anaerobic training and that would be a boxer. This just ain’t from my love of the sport and admiration for boxers - but if you think about how they train, this article would make sense. Am I correct in thinking this?

Boxing or other interval type sports are good examples of high intensity work, but are much harder to explain because I would have to talk about recovery VO2 (also known as O2 deficit or excess post-exercise oxygen consumption (EPOC)). But that is beside the point. If I could boil down this post into one thought it would be this: when you increase cardiovascular exercise intensity, you burn more calories and there is a shift towards a larger percentage of calories coming from carbohydrates, BUT NOT AT THE EXPENSE of fat utilization. For example, you could train at a low intensity and burn 10 cals/minute (say 5 from fat and 5 from carbs) or you could up the intensity and burn 20 cals/minute (8 from fat and 12 from carbs (8 aerobically and 4 anaerobically). Once again, these are just example calculations, but I want to help dispell the fat-burning zone myth. This fat-burning zone is taught as like 50-70% max heart rate, but this is a lie perpetuated by the generally accepted theory that as RER increases, you are burning less fat and more carbohydrate. That is not what I think. As RER increases you are burning more calories, more fat aerobically, more carbs aerobically, and even more carbs anaerobically. The only reason the RER is changing is due to anerobic CO2 production. If that was taken out, you would see a very consistent RER. Unfortunatly, there is no technique to account for this and you cannot measure what is actually going on at the cellular level, so the RER is our best estimate for the RQ. But take my word for it, the RER is not equal to the RQ, aside from maybe resting conditions.

In terms of practical application to physiques (which is what this forum is all about, afterall), this can be best seen in Australian Rules Football players. There are some incredibly huge guys with amazingly low body fat percentages and some of the highest aerobic capacities around, playing AFL. I’m sure many of us would be more than content with some of the physiques these guys have in terms of size, yet they do an awful lot of cardio. Sure, they are often blessed with genes we could only dream of, but that doesn’t hide the fact that cardio isn’t as bad as its often made out to be.

Thanks for clarifying. Maybe than a test should be performed on a athlete from the following backgrounds: boxing, bodybuilding, soccer and/or football and powerlifting. And maybe a marathon runner as well. The question I always ask is if a test was performed to prove these theories and if that was the case, who particpated in these tests? Just regular ole’ people? Or athletes. Because don’t athletes, after a while of hard training, start burning “fuel” more efficiently? I know that after playing soccer for 8-years in my school-girl years, and right after becoming involved in weight training, and then martial arts as well as several different physically active activities (including Jazz dancing…go figure) - my body now burns more efficiently. It would take ALOT for me to get all fat. I’m really simplifying what is being discussed here - I do apologize. I’m not trying to diminish this thread at all - but this is what I got to do. So - is what you’re saying based on someone who is at the beginning of a physically active stage or in the middle or has been physically active for quite sometime? But I would like someone to perform this test on the different athletes I earlier mentioned - that would be interesting.

Patricia - This theory was devised with data of around 100 subjects or so and these subjects ranged from athletes to normal people. In response to your proprosition that athletes burn fuel more effeciently, I think that you somewhat contradict yourself. For an athlete to burn fuel more efficiently, that would mean that they can do more work (exercise) on less fuel. You seem to indicate that athletes have a much higher metabolic rate overall, which does not mean that they burn fuel more efficiently, but rather that they require more fuel to maintain body weight. I think that as an athlete plays a certain sport for years, he learns how to play smart. He does not waste energy on the field or on the court. This would mean that the athlete expends his voluntary energy more efficiently rather than burning fuel more efficiently. BTW, to do a certain amount of work takes a certain amount of energy. For instance, if I set a cycle ergometer to a workload of 200 watts, it would take the same caloric expenditure for you, me, a sedentary person, Ronnie Coleman, and a skinny marathon runner. Obviously, it would be easier for some than others, but we would all be expending about the same calories to turn the pedals. Overall though, the point that I was trying to make is that the so-called fat burning zone does not exist. As exercise intensity increases, you burn more fat. Unfortunately, if you consult any typical exercise physiology textbook, you will see that the authors say that there is a point at which you hit maximal fat burning and if you increase workout intensity beyond that, you will start burning less fat and more carbs in place of this. I do not believe this to be the case.

I first started hearing about this from barry sears. I was heavily into the zone at the time and I got alott of studies sent to be on anerobic vs aerobic training, and especially muscular triglicerides conributing to anerobic events. I beleive their was a study done by Estan Gustaven that shows tgs application to weight lifting.

Good thread, BUT as exercise intensity increases does not lipolysis become inhibited through Malonyl CoA, as well as oxygen kinetics not being able to keep up and the recruitment of fast twitch fibres that are low in mitochondria all leading to a greater use of glycogen as fuel. I am not stating these as definites but would like to hear your opinion on them.

Good thread, BUT as exercise intensity increases does not lipolysis become inhibited through Malonyl CoA, as well as oxygen kinetics not being able to keep up and the recruitment of fast twitch fibres that are low in mitochondria all leading to a greater use of glycogen as fuel. I am not stating these as definites but would like to hear your opinion on them.

Regarding the oxygen kinetics portion of your question, as long as you increase workload intensity slowly, O2 kinetics is not an issue. If you head out to the track and jump right into near maximal work, you will rely primarily on anaerobic metabolism until you catch up aerobically. This of course creates an O2 Deficit that will be payed back after exercise with excess post exercise oxygen consumption. Either way (slow increase or jump into near max training), you are going to utilize a lot of fat and carbs. In regards to the increase recruitment of fast-twitch glycolytic fibers, you are correct in assuming that these fibers will use glcogen rather than fat, but this does not contradict what I have said earlier. As exercise intensity increases, both aerobic and anaerobic energy expenditure increase. Some of and sometime as significant portion of the anaerobic energy expenditure is a result of fast-twitch fiber recruitment. Now, finally in regards to malonyl-CoA. An increase in malonyl-CoA would begin to inhibit fatty acid utilization, but to what extent this occurs during exercise, I am not sure. From the studies that I have just looked up, I would tend to think that malonyl-CoA decreases during exercise and thus would allow for greater fatty acid utilization. From (Elayan and Winder, JAP, 70(4), 1991, pp. 1495-1499)-Malyonyl-CoA, the first committed intermediate in the conversion of glucose into fat inhibits carnitne palmitoyltransferase I thus inhibiting fatty acid transfort into the mitochondria, meaning we would not burn fat. When glucose is very abundant and being converted to fatty acids, malonyl-CoA production increases. When glucose decreases, malonyl-CoA decreases. From (Winder et al., JAP, 67(6), 1989, pp. 2230-2233), experimental results demonstrate that malonyl-CoA decreases during exercise before depletion of muscle and liver glycogen and before blood glucose drops. Anyway, I don’t believe malonyl-CoA increases during exercise. Do you have evidence to the contrary? If you do, I would love to look it up. I know that I did not cite things in the most proper form, but I think that you should be able to look up those articles and see for yourself. One final note, rats were used as the experimental subjects in these trials. We all know that humans are not rats. I just could not find any human studies in the short time I spent researching your question.

Bumping this thread up for british lifter before it gets lost in the forum dungeon. If you’re out there, I was curious if you had any evidence that malonyl-CoA is elevated in humans during high intensity cardiovascular exercise.

Jason N, I was reciting from memory an old Exercise physiology lecture and I cant find my notes to find the references that the lecturer quoted- I’ll find them eventually and post them on this thread or start another.

Jason, I want to commend you for a nice post. I usually don’t post, because a lot of what’s here is what we call “arm chair science” and it takes a lto of time. I met Dr. Mole, and I regret now not talking to him more.

Regarding your post, you sound kind of like me in class! I like some of your calculations, that make it easier for non science students to understand.

You mention as intensity increases, more CHO are used, but not at the expense of fat utilization. This depends on exercise intensity (EI) though. Looks like you are referring to EI, below lactate threshold (LT), because above LT fat utilization will drop. You usually don’t see RER’s of 1.2 at LT. And yes RER may not the best way to demonstrate this. Let me explain.

Lipolysis is definitely not limiting during exercise at any intensity and the reduction in blood flow (with the albumin contained in blood) limits how much FFAs can be transported/removed from the adipose tissue. For example, we know that immediately after exercise there is a very large increase in the rate of appearance of FFA into the blood stream - due entirely to blood flow being restored to the adipose tissue. So the theory is that the increase in epinephrine and blood flow during submaximal exercise activates HSL with the subsequent increase in the rate of appearance of FFA into the blood. As exercise intensity becomes very intense the increase in sympathetic activity apparently causes vasoconstriction of blood vessels going to adipose tissue. But this does not explain the reduction in fatty acid oxidation since infusing intralipid (to keep free fatty acid concentration very high) during intense exercise does not prevent the reduction in FFA oxidation. The predominant reason is most likely inhibition of FFA oxidation in skeletal muscle via inhibition of CPT. But we also know that malonyl-CoA content does not increase (as some have speculated that increased glycolysis and hence acetyl-CoA would stimulate acetyl-CoA carboxylase and cause malonyl-CoA levels to rise) to cause CPT inhibition. So other factors such as increased H+ concentration or increased acetylcarnitine may be the inhibitors of CPT during intense exercise.

But remember that even though we say there is a reduction in fat oxidation during intense exercise we are simply comparing intense vs. submax exercise. If you compare resting
rates of FFA oxidation vs intense exercise rates of FFA oxidation we still see a 5-6 fold increase in total FFA oxidation during intense exercise. The reduction of malonyl-CoA with subsequent removal of CPT inhibition probably
plays a major role in this…and then the drop in pH and other metabolites may partially inhibit CPT activity causing some suppression (in addition to reduced FFA availability) of FFA oxidation as compared with the rates
measured during submaximal exercise.

The way I say it to my students is very similar to what you have said, that is that as RQ (RER) increases, more CHO is used relatively (as a %) and less fat is used. However more absolute fat is used, as long as the bout is not duration limited (above LT), where the items mentioned above come in to play.