EPOC and the Neuroendocrine Response

[Pat McElhone]

In Steven Low's article states " EPOC (excessive post-exercise energy consumption) has generally been the explaining for the phenomena superior fat loss for HIIT versus ET. This theory is incorrect". I read the pubmed abstracts of the study this was based on (Laforgia, et al. 2006) and the related studies in Pubmed and have the following questions/points of view/thoughts.

1. How was EPOC measured? The abstracts did not say. How does on measure oxygen (O2) consumption? O2 Uptake can be measured easily, was this measured? If one only looks to when O2 uptake returns to normal, this does not correlate to when O2 consumption returns to normal. O2 uptake and O2 delivery (DO2) are generally 3-10x in excess of O2 needs (MVO2). So, you can have O2 uptake return to normal, but still have elevated O2 consumption.

2. How was "EPOC comprises only 6-15% of the net O2 cost of exercise" determined? Again, did they look at how much O2 was uptaken during exercise and after how long until O2 uptake returned to normal?

3. The neuoroendocrine response to exercise results in both an increase in Beta oxidation and glycolysis. The purpose of both of these is energy production (ATP). Beta oxidation gives us the substrates NADH, FADH2, and Acetyl Co-A. Beta Oxidation requires O2 (O2 consumption). Next, glycolysis also gives us a small amount of ATP, but also substrate (pyruvate), which ulitmately leads to NADH and FADH2. NADH and FADH2 require O2 (more O2 consumption) to give us ATP (energy). Is this O2 consumption considered as part of EPOC?

I just do not see how someone can measure O2 consumption or really how O2 consumption (not uptake) can be separated from the oxidative phosphorylation. Finally, when the term EPOC was "coined" does anyone know how it was used? Was it meant to refer not just to O2 consumption, but beta-oxidation, glycolysis, oxidative phosphorylation?

All points of view are welcomed. It is nice to find an environment where my main interests....exercise and physiology/pharmacology interact. Now if anyone wants to start a thread on Alpha-2 receptors, I am in :)!

[Mike ODonnell]

Now if anyone wants to start a thread on Alpha-2 receptors, I am in :)!

That would be a good one!....although we need to bring back the ECA stack first.

[Pat McElhone]

That would be a good one!....although we need to bring back the ECA stack first.

New here, what is the ECA stack?

[Dave Van Skike]

You know..I find the whole ephedrine caffeine aspirin (ECA stack) combo to be more believable and demonstrable than either EPOC or "neuroendrocrine response"....talk about black boxes

In fact... I think conceptually they're both slightly less useful than other training myths like the gallon of milk a day and the 20 rep squat, which deliver results nearly every time but are based on some pretty crude assumptions.

[Steven Low]

I would *assume* the studies were smart enough to measure both O2 and CO2 as well as other methods. I think myoglobin storage of O2 is one of the reasons for the variable calculations as well as other estimates. For example, if you're interested in different methods take a look at this study on 400m/800m "anaerobic" vs "aerobic" contribution:

http://www.ingentaconnect.com/content/tandf/rjsp/2005/00000023/00000002/art00010

I do not know which one that used specifically though so I'm more or less dependent on the veracity of the researchers methods as much as you (unless you're willing to purchase the study o_o).

As for #3 I am sure they took that into account if not solely on the fact that the researchers did not even know about that. With global measurements, distinguishing O2 consumption is pretty much impossible which it should be as all O2 consumption (for ATP) should be considered EPOC.

Most of the oxygen consumed, ultimately would be for increased production of ATP from the result of oxidative phosphoylation from adipose tissue stores. That's because of the abundance of NADH that it produces so ironically or not even though interval training is traditionally assumed as "anaerobic" EPOC or any type of O2 consumption is measured mostly through aerobic contribution.

Sorry I don't have much more view into it than you do although I would check out the different methods of analysis in the paper I listed above to see if they hold up. Odds are they used one of them because if they used a new method of measurement they would've probably noted it in the abstract (and described it as well so it would show up in databases better and their article would get more hits/references).

[Pat McElhone]

I am not ready to make the same assumptions. In fact, I assume O2 consumption was measured by looking at O2 uptake (ViO2, as termed in the linked article), versus O2 exhaled (VeO2), ViO2:VeO2 and when these values returned to baseline. Measuring tissue oxygenation is hard and expensive.

The linked article measures 4 things, with only lactate and ViO2 being quantitative data. One could argue that looking at lactate production can give insight into aerobic verses anaerobic ATP production, but with a total N of 16 and 11, how much is a natural variance? When I analyze a study and I see the term "calculated", I think "estimated".

I am surprised there is not a "Journal Club" topic on this board. People could post an interesting study and we could all tear it apart frequently or on a rare occasion, say "wow, a study that might actually prove a new thing that is actually applicable!"

Steven, thank you for the post, links, articles, your enthusiasm is nice to see.

[Steven Low]

Yeah, that's the problem with pretty much 99% of the studies coming out in exercise science/physiology... they have control/experimental groups of <15 people. Very small sample size doesn't lead to a great bit of accuracy in the data.

Yeah, sorry I can't offer anymore. Besides the Laforgia study you might be able to find a full text within the first couple links on EPOC I provided. I believe there was at least one.