Energy deficit w/o LC alters resting carb oxidation and FA availability

Originally lucky post #13 made on March 23, 2010

In light of all of the "fat burning" , respiratory quotient and mitochondrial mayhem discussions of damaged metabolisms, I thought this might be a fitting post to bump to the top today.  The take home message of this study, IMO, is that the body burns what it needs to burn, and hormone levels adjust accordingly, not so much the other way around.  

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Energy deficit without reducing dietary carbohydrate alters resting carbohydrate oxidation and fatty acid availability

Reduced carbohydrate (CHO) availability after exercise has a potent influence on the regulation of substrate metabolism, but little is known about the impact of fat availability and/or energy deficit on fuel metabolism when dietary CHO availability is not reduced. The purpose of this study was to determine the influence of a postexercise energy deficit, independent of CHO availability, on plasma substrate concentrations and substrate oxidation.

Seven moderately trained men (peak oxygen uptake: 56 ± 2 ml·kg–1·min–1) performed exhaustive cycling exercise on two separate occasions. The two trials differed only by the meals ingested after exercise: 1) a high-fat diet designed to maintain energy balance or 2) a low-fat diet designed to elicit energy deficit. The CHO and protein contents of the diets were identical. The next morning, we measured plasma substrate and insulin concentrations and CHO oxidation, and we obtained muscle biopsies from the vastus lateralis for measurement of pyruvate dehydrogenase kinase (PDK)-2 and PDK-4 mRNA expression by using RT-PCR.

Despite identical blood glucose (5.0 ± 0.1 and 4.9 ± 0.1 mM) and insulin (7.9 ± 1.1 and 8.4 ± 0.9 µU/ml) concentrations, plasma fatty acid and glycerol concentrations were elevated three- to fourfold during energy deficit compared with energy balance and CHO oxidation was 40% lower (P < 0.01) the morning after energy deficit compared with energy balance (328 ± 69 and 565 ± 89 µmol/min). The lower CHO oxidation was accompanied by a 7.3 ± 2.5-fold increase in PDK-4 mRNA expression after energy deficit (P < 0.05), whereas PDK-2 mRNA was similar between the trials.

In conclusion, energy deficit increases fatty acid availability, increases PDK-4 mRNA expression, and suppresses CHO oxidation even when dietary CHO content is not reduced.

The theory part of this article is fairly lay-person friendly so I encourage reading it.

I found this very interesting.  I only wish they had added a third meal for comparison -- that being a high fat/low carb energy deficit diet. 

Each phase of the study lasted 2 days.  They got a standard meal to eat for dinner the night before the study.  On Day 1 resting data was collected, they exercised to exhaustion, and were then given a diet to be eaten in 3 equal portions afterwards.  The study diet consisted of 1.1g/kg protein and 5g/kg carbohydrate, ~165g fat was added to the energy balance "high fat" diet, while the energy deficit diet contained ~1500 cal less.  Resting data was collected on Day 2.

This study demonstrates that the energy deficit, independent of carb ingestion, dramatically alters the post exercise response of energy substrate usage.  And this was over a 24 hour period.  Here are the plasma lipid levels (click on the pic to enlarge):

The increased glycerol and NEFA/FFA are the result of increased lipolysis of endogenous (body!) fat.  Interestingly enough, the insulin was reduced from Day 1 but the same in both groups.  Changes in IL-6 were not statistically significant although they do seem to trend up and become more variable in that energy balance group.

And lastly, the carbohydrate and fat oxidation rates:

*Significantly different from energy balance trial, P < 0.05.  

{dagger}Significantly different from day 1, P < 0.05.

So exercising to exhaustion changed energy substrate usage (daggers indicate stat.sig. differences from Day 1) in both groups.  Carb oxidation is reduced while fat oxidation increases.  The fat oxidation increaase is greater in the energy deficit group!!

Now these men weighed ~76 kg so both diets contained >300g carbohydrate!  An amount that Taubesians would presume sends insulin levels through the roof, locks fat into our cells and should send blood glucose levels and triglycerides through the roof. 

From the Discussion :

An acute energy deficit triggers essential metabolic alterations to mobilize endogenous lipids and preserve endogenous carbohydrate when exogenous energy availability is low (2, 26). However, because carbohydrate availability provides a potent influence on substrate selection, it is often very difficult to distinguish between the effects of energy deficit and carbohydrate restriction. The major finding of this study was that, without reducing dietary carbohydrate availability, an exercise-induced energy deficit increased plasma fatty acid concentration and suppressed carbohydrate oxidation. Moreover, compared with an exercise-induced energy deficit, maintaining energy balance by ingesting extra dietary fat after exercise (without changing dietary carbohydrate content) prevented the rise in plasma fatty acid concentration and attenuated the decline in carbohydrate oxidation the next morning.

Exercise-induced energy deficit is known to suppress carbohydrate oxidation (1, 40). However, because the human body is keenly sensitive to alterations in dietary carbohydrate, much of this effect has been attributed to the reduction in dietary carbohydrate and the resultant low liver and muscle glycogen resynthesis, rather than the negative energy balance. Providing identical carbohydrate content during energy deficit and energy balance in our study enabled us to differentiate between the effects of energy deficit and the known potent influence of alterations in dietary carbohydrate (8, 16, 43). This study is the first to demonstrate that preventing energy deficit after exercise by ingesting extra dietary fat attenuated the reduction in carbohydrate oxidation. Interestingly, this attenuation in carbohydrate oxidation the day after exercise was found despite identical plasma insulin and glucose concentrations during energy deficit and energy balance. Furthermore, in a companion study to this project using these same subjects (13), we found that adding extra dietary fat to meals after exercise did not affect muscle glycogen resynthesis. These findings indicate that the reduction in carbohydrate oxidation during energy deficit is not solely dependent on plasma insulin concentration or endogenous and exogenous carbohydrate availability, but that it can respond to dietary fat and/or energy availability, per se.

Now this study was done in moderately trained, healthy, young (~30y) men.  But this does demonstrate that insulin is not the be all and end all of fat burning.  The energy deficit increased the relative changes in substrate oxidation (carb down, fat up).