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.
