Metabolic Flexibility: You Need to Burn That Fat Off!
Large and In Charge Mouse
I hope all of you got to watch the Vikings win this past Sunday! Whoo ha!!
Onward to today’s topic of Metabolic Flexibility.
What is that and why do I care?
Physiology is Messy
Physiology is complex and messy. Most theories just don’t hold up since they are too simple. Note, this does NOT mean that the actions you need to take have to be complex, but the theory to explain all the inter-workings gets complicated at times.
Metabolic Flexibility (Met Flex) is the term to describe the ability of the body to burn both fats AND carbs efficiently.
Enter the Diabetic Stage Left
The basic definition of a diabetic is someone who does not handle carbs (carbohydrates) very well. Their glucose management has gone awry and is messed up. Don’t get me started on why the popular recommendation is then for diabetics is truck loads of CARBS! Ok, just a short rant since it is my blog and I read research studies for fun.
Now to be entirely fair, the American Diabetes Association (ADA) has cracked the door a bit to low-carb diets for people with diabetes and pre-diabetes (and insulin resistant) but for weight control ONLY and it doesn’t recommend low-carb diets for blood glucose control, even though the new guidelines say,
“dietary carbohydrate is the major determinant of postprandial [after meal] glucose levels”.
If you are a diabetic or borderline diabetic, dumping a crap ton (technical term) into your system of the very thing that you have a hard time processing, is a bad idea.
Toxic Sugar
Keep in mind that HIGH level of glucose (sugar) in the blood is TOXIC. Low levels are also bad, so the body has tons of controls to keep you at a happy medium (homeostasis for my fellow geeks). The downside is that some of these short term controls (read, so you don’t die) come at a very high cost long term (read: destruction of other tissues).
Fat Metabolism: Torch the Muffin Top
In the USA, Even the Wild Animals Are Now Fat!
source: James Marvin Phelps (mandj98)
On the other end of the spectrum, although not as common, are people who can’t handle high amounts of dietary fats. The machinery that processes fat has gone off the tracks and this too results in lots of collateral damage.
Summary So Far
So those are the bad circumstances
1) poor handling of carbs
or
2) poor handling of fats
For all practical purposes, the burning of protein as a fuel does not happen that much; despite all the fear mongering of bro-scientists everywhere in the bodybuilding circles.
Now, some poor bastards can have BOTH (fat and carb metabolism) gone awry and are an unfortunate metabolic wreck.
The Good Side
So if that is the bad side, people who are very metabolically INflexible to fats and carbs; there is a good side - people are who very metabolically flexible to carbs and fats. This is where you want to be.
You want the ability to handle fats AND carbs without any collateral damage and increase your health and performance.
How?
The most profound effector of this is ………EXERICSE! Any surprise there? A high levels of exercise, your body becomes very efficient at handling fats AND carbs (2). There is accumulating evidence (1) that lower levels of body fat are also correlated to metabolic flexibility. We used to think that fat cell sat around on their collective fat butts all day, but we now know they run a host of chemical messengers throughout the body. Fat as it turns out is very metabolically active (think busy fat cells not lazy ones).
Metabolically Flexible Robots? What?
KITT from Knight Rider: A Smart Robot
Now I don’t believe much of anything I read on Fox news, but there was a story about the military making new robots that can eat anything. Sweet! A metabolically flexible robot! I always knew DARPA was ahead of us.
from Fox News (yeah I know, I am quoting fox news, eeek)
“Robotic Technology Inc.’s Energetically Autonomous Tactical Robot — that’s right, “EATR” — “can find, ingest, and extract energy from biomass in the environment (and other organically-based energy sources), as well as use conventional and alternative fuels (such as gasoline, heavy fuel, kerosene, diesel, propane, coal, cooking oil, and solar) when suitable,” reads the company’s Web site.”
You gotta love the name too EATR. ha! For those that want to see the whole presentation on EATR, I tracked it down and you can get it HERE.
Are the Robots Ahead of Us?
It is time to add some more exercise and get more metabolically flexible soon, before a robot comes looking to eat you for lunch. This also has a great side effect of decreasing that spare tire and muffin top too.
Sprints anyone? Catch me if you can you lazy robot!
Rock on
Mike T Nelson
PS
For those that are interested in this topic, hold on to your hats as I have a whole product coming out soon called “The Truth about Protein, Fats, and Carbs: Implications for Metabolic Flexibility” I am also in the process of writing up some studies for peer review on metabolic flexibility (silly dissertation).
REFERENCES
1) MITOCHONDRIAL RESPIRATION IS INCREASED FOLLOWING
LIPID EXPOSURE IN CULTURED MYOTUBES FROM LEAN BUT
NOT OBESE DONORS
Appl. Physiol. Nutr. Metab. Vol. 34, 2009
Boyle KE, Zheng D, Anderson ET, Neufer PD, & Houmard JA. Dept.
of Exercise & Sport Science & The Metabolic Institute, East Carolina
University, Greenville, NC
The skeletal muscle of obese humans oxidizes less lipid compared to
leans and is unable to respond to a lipid challenge. We utilized satellite
cells derived from vastus lateralis tissue of 7 lean (BMI=22) and 8 obese
(BMI=38) human males to determine the mechanisms involved with
the inability to utilize lipid with obesity. On day 6 of differentiation,
myotubes were incubated in differentiation media supplemented with
either 100?M oleate/palmitate + 0.05% BSA or 0.05% BSA for 24h. Cells
were then permeabilized and state 4, state 3, and uncoupled respiration
was measured in the presence of palmitoyl carnitine + malate (+succinate
for uncoupled). State 3 and uncoupled respiration increased in leans with
the lipid incubation (50% & 35%, respectively; P<0.05). There was no
corresponding change in the cells from obese donors. Mitochondrial
DNA copy number increased in leans but decreased in obese with lipid
incubation (16% & -13%, respectively; P<0.05) and COX-IV protein
content showed a significant lipid incubation x body size interaction (38%
increase in leans and -13% decrease in obese; P<0.05). These data suggest
that the skeletal muscle of obese individuals does not respond to lipid
exposure by increasing lipid oxidation; this metabolic inflexibility may be
a mechanism involved in the reduced ability to oxidize lipid evident in the
muscle of obese subjects.
Funded by NIH DK561112 & DK073488.
2) ADAPTATIONS IN NR4A3 ISOFORMS FOLLOWING EXERCISE
TRAINING IN OBESE HUMANS
Appl. Physiol. Nutr. Metab. Vol. 34, 2009
Haus, J.M., Solomon, T.P., Kirwan, J.P. Cleveland Clinic, Cleveland, OH
The orphan nuclear receptor NR4A3 responds to acute exercise and
has been implicated in the regulation of genes that mediate glucose
and lipid metabolism in skeletal muscle. Data on the effects of exercise
training on NR4A3 gene expression are lacking. We examined mRNA
expression of the known NR4A3 isoforms (A,B,C) from muscle biopsy
samples obtained at basal and under insulin stimulated conditions (INS)
during a 40 uU/m2/min hyperinsulinemic-euglycemic clamp before and
after 12 weeks of aerobic exercise training. Subjects included obese
men and women. At baseline, NR4A3 isoform C was most abundant
(2.7±1.1, 3.5±1.4, 5.6±1.7 AU), and INS increased expression of all three
isoforms (3.4, 1.6, 4.7 fold; P<0.05). Exercise training increased basal fat
oxidation, glucose disposal rates (GDR) and basal mRNA expression of
NR4A3 isoforms B and C (1.4 and 2.1 fold; P<0.05 vs. pre). In addition,
the expression of NR4A3 isoforms A, B and C were decreased during INS
(-55, -29, -61% vs. Pre INS). Following exercise training, increased basal
expression of NR4A3 isoforms B and C may reflect the increase in basal
whole body fat oxidation. The exercise-induced attenuation of NR4A3
gene expression during INS is consistent with the observed improvements
in metabolic flexibility following exercise training. These novel data
provide evidence that NR4A3 may regulate glucose and lipid metabolism
following exercise training in obese, insulin resistant adults
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