What is metabolism? Exercise professionals and educated exercise
professional have posed numerous theories, facts, and understandings of what
metabolism is. We can look/read any magazine, website, or blog related to
fitness and weight loss and find information pertaining to "facts"
about metabolism. And although they all share commonalities, how specific,
reliable, and most importantly valid are these '"facts". To
truly understand, let us define metabolism based on what I call "pop
exercise" literature. According to numerous sites...... (Which will remain
nameless....hint Google metabolism), metabolism is "the rate in which your
body burns calories".....Clearly it’s that simple folks. Surprisingly, if
you ask any fitness professional you will get this answer, but who cares right?
If you can promise them weight loss, the client/individual does not need to
know anything but that. Well readers, that is crap. How are we supposed
to promise achievement of goals if we do not understand or just do not know
what the internal processes entail? And what about these things we read all
over the place and in all form of media promoting programs to "kickstart"
metabolism, or even hear from fitness professionals that certain diets will
"increase metabolic rate(s)".....news flash, there is no such
thing.
So let's start truly understanding what metabolism is. First and
foremost, we need to stop referring to metabolism as a singular entity, but
instead an amalgamation of processes that occur during ANY type of activity (Rowe,
P. (2012)). For example, your sleep cycle, resting (basal),
anabolic/catabolic functions, cardiac, pulmonary, etc. Metabolic output,
regardless of individual size, weight, height, age are the SAME (Hamidi, T.,
Algül, H., Cano, C., Sandi, Et al, 2012).
Ultimately the end result of all metabolic processes is the same. The
changes only occur during each individual metabolic component; the efficiency
of each system (Hamdi, M., & Mutungi, G. 2011).
For example the cardiac metabolic efficiency
of a 250lb man may be different than that of a 150 lb man, thus the cardiac metabolic
efficiency is greater with the 150lbs man. But regardless, the different
components of the metabolism will equate the end result via utilization of
other systems (Kravchenko, L., Aksenov, et al 2012).
Let’s focus on more specific metabolic processes. It’s interesting that when
metabolism is brought into conversation, calories are automatically
related….well first of all, what is a calorie? Calories are the amount of
energy necessary to heat 1 gram of water to 1 degree Celsius……so why is a unit
of energy the focus? These units of energy are utilized regardless of activity,
it’s the conversion of each unit to fat that becomes an issue, but if you are
exercising, you should not have a problem. So why is a unit of energy a
focus…the simple answer is that it should not be. Although it is an important component,
why should it be the priority? According to Kravchenko, L., Aksenov, et al
2012, metabolism instead is a function of O2 uptake efficiency.
Metabolic functions, regardless of the fuel
are highly dependent on the utilization of O2. To simply put, the increased
efficiency of metabolic function has a direct relationship with exercise
performance and metabolic efficiency. The better you breathe, the more
efficient your body becomes.
Now what is this nonsense about thermogenics and metabolism? Does increasing
internal temperature create a better “burn”? When you workout hard and you
start sweating, that means that my metabolism is working hard right?.......well
folks that’s CRAP……for the most part.
Let me clarify this for all you readers through logical, valid,
reliable, and scholarly literature.
Your
body goes through a series of metabolic efficiency and deficiency know as
catabolic and anabolic functions (Dixon,
L., Berk, M., Thapaliya, S., et al 2012). During anabolic efficiency, your body
is rebuilding…..it is in a state of repair. When you are working out….your body
goes through a process called catabolism.
This is when your body is breaking down and using those units of energy
called calories. Heat is produced during the anabolic phase….the phase of
repair. Ultimately your internal core temp increases at rest. So your
temperature (internal) has no bearing on how much you expend!!!
And why would you want to chemically increase
your internal temperature in the first place? During anabolism, your body
utilizes your synthesized proteins…..the funny thing about proteins; they
denature and become useless after X degrees. You just wasted your workout.
As educated professionals, we need to stop using the word metabolism, and
replace it with efficiency. We need to become more educated in all aspects of
exercise physiology and not have this constant tunnel vision on one modality of
exercise.
Understanding mechanics and
proper form is great, but to truly program a person for success, we need to
have an understanding of why we are prescribing programming and why we are
giving specific advice; not only superficially, but deeper and more specific.
WHICH BRINGS ME TO MY NEXT TOPIC……H20….
TUNE IN NEXT WEEK, AND HAPPY EXERCISING!!!
Citations:
Rowe, P. (2012). Regulation of bone-renal mineral and energy metabolism: the
PHEX, FGF23, DMP1, MEPE ASARM pathway.
Critical Reviews In Eukaryotic Gene
Expression,
22(1), 61-86.
Dixon, L.,
Berk, M., Thapaliya, S., Papouchado, B., & Feldstein, A. (2012).
Caspase-1-mediated regulation of fibrogenesis in diet-induced steatohepatitis.
Laboratory
Investigation; A Journal Of Technical Methods And Pathology,
92(5),
713-723. doi:10.1038/labinvest.2012.45
Zhang, Y., Babcock, S., Hu, N., Maris, J., Wang, H., & Ren, J. (2012).
Mitochondrial aldehyde dehydrogenase (ALDH2) protects against
streptozotocin-induced diabetic cardiomyopathy: role of GSK3β and mitochondrial
function.
BMC Medicine,
1040.
Hamdi, M., & Mutungi, G. (2011). Dihydrotestosterone stimulates amino
acid uptake and the expression of LAT2 in mouse skeletal muscle fibres through
an ERK1/2-dependent mechanism.
The Journal Of Physiology,
589(Pt
14), 3623-3640.
Kravchenko, L., Aksenov, I., Trusov, N.,
Guseva, G., & Avren'eva, L. (2012). [Effects of dietary fat level on the
xenobiotic metabolism enzymes activity and antioxidant enzymes in rats].
Voprosy
Pitaniia,
81(1), 24-29.
Hamidi, T., Algül, H., Cano, C., Sandi, M., Molejon, M., Riemann, M., &
... Iovanna, J. (2012). Nuclear protein 1 promotes pancreatic cancer
development and protects cells from stress by inhibiting apoptosis.
The
Journal Of Clinical Investigation,
122(6), 2092-2103. doi:10.1172/JCI60144
Ghosh, A., Wang, B., Pozniak, C., Chen, M., Watts,
R., & Lewcock, J. (2011). DLK induces developmental neuronal degeneration
via selective regulation of proapoptotic JNK activity.
The Journal Of Cell
Biology,
194(5), 751-764.
Wang, A., Dorso, C., Kopcho, L., Locke, G., Langish, R., Harstad, E., &
... Kirby, M. (2012). Potency, selectivity and prolonged binding of saxagliptin
to DPP4: maintenance of DPP4 inhibition by saxagliptin in vitro and ex vivo
when compared to a rapidly-dissociating DPP4 inhibitor.
BMC Pharmacology,
122.
Strutyns'kyĭ, R., Kotsiuruba, A., Neshcheret, O., Rovenets', R., &
Moĭbenko, O. (2012). [The changes of metabolism in myocardium at
ischemia-reperfusion and activating of the ATP-sensitive potassium channels].
Fiziolohichnyĭ
Zhurnal (Kiev, Ukraine: 1994),
58(1), 13-26.