A Proactive Choice For DiabetesDiabetes – A Silent Storm According to the American Diabetes Association, 23.6 million people in the US have diabetes, or about 7.8% of the population1. What Does Diabetes Cost The US…Cost You? The American Diabetes Association reports: www.diabetes.org/diabetes-statistics/cost-of-diabetes-in-us.jsp
What Is Diabetes Type II? Type II is the most commonly diagnosed form of diabetes. This is when insulin resistance develops, meaning the cells’ ability to take glucose from insulin decreases. As a result, more insulin is produced, blood glucose levels rise, and if it isn’t addressed soon, the individual may develop type II diabetes. Type II diabetes is one of the major heart disease risk factors. Ideally, the excess blood sugar (glucose) will go to extra storage space in the cells of the liver or muscles. The liver is typically filled, and the muscle cells mostly contain glycogen (the stored form of glucose) for energy use. If the muscle cells are filled, then insulin will go to its third and undesired destination, adipose (fat) tissue. This is when insulin resistance develops. In essence, glucose is either brought to fat cells for storage or left in the blood…neither of which is desirable.
SuperSlow® Strength Training Is THE RIGHT CHOICE! How can SuperSlow® strength training play a role? Studies show strength training to increase insulin sensitivity 2 3(the condition where cells are more able to take glucose from insulin) and decrease blood glucose levels3. Strength training is mainly fueled by an energy cycle called anaerobic metabolism. The higher the intensity, the more frequently this cycle occurs. What is the material used at the start of this cycle? Glucose. In addition, muscle tissue is the major desired storage space, holding roughly three times the glycogen that the liver can. High intensity strength training, such as SuperSlow®, leads to the production of the stress hormones epinephrine and norepinephrine. When this emergency preparation response occurs, muscles release significant amounts of glycogen, which can then be used for energy. In addition, high intensity strength training produces enzymes that remove molecules of glucose from muscle stores. These enzymes activate other enzymes at an exponential rate, meaning tens or hundreds of enzymes will each be removing glucose4. While this breakdown and removal of glycogen from muscles occur, enzymes block the creation of more glycogen. Basically, glycogen is being released but can’t be synthesized4. Muscle Loss – Sarcopenia Finally, consider this: We lose muscle as we age…a lot of muscle. The Mayo Clinic reports that we lose about 1% of our muscle mass every year after 305. How does this relate to diabetes? Less muscle means becoming less adept at storing blood sugar. It’s no wonder that type II diabetes is known as “adult onset diabetes”. The good news is that this loss can be stopped and reversed with a small amount of high intensity strength training every week. Rebuild your muscles to a youthful state. Keep glucose away from your fat cells. Keep your blood sugar at a healthy level. Do SuperSlow® strength training! Sean Preuss 1 “All About Diabetes.” American Diabetes Association. 22 May 2009 http://www.diabetes.org/about-diabetes.jsp 2 Cauza, E., Hanusch-Enserer, U., Strasser, B., Ludvik, B., Metz-Schimmerl, S., Pacini, G., Wagner, O., Georg, P., Prager, R., Kostner, K., Dunky, A., Haber, P., “The relative benefits of endurance and strength training on the metabolic factors and muscle function of people with type II diabetes mellitus.” Archives of Physical Medicine and Rehabilitation 88, no. 3 (March 2007): 397 3 Holten, M. K., Zacho, M., Gaster, M., Juel, C., Jorgen, F. P., Wojtaszewski, Dela, F., “Strength Training Increases Insulin-Mediated Glucose Intake, GLUT4 Content, and Insulin Signaling in Skeletal Muscle in Patients with Type 2 Diabetes.” Diabetes 53, no. 2 (February 2004): 294-305 4 McGuff, Dr. D., Little, J. “Global Metabolic Conditioning.” Body by Science. McGraw-Hill, 2009. 20-34. 5 “Sarcopenia.” Mayo Clinic Health Letter, February (2002): page 7. |
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