There is a genetic predisposition to onset of diabetes but physical inactivity is at odd with our nomadic gene and may increase the risk of type 2 diabetes. The term insulin resistance is the main driver for onset of type 2 diabetes. It is defined as a condition in which the body produces insulin but the insulin sensitive organs (liver, adipose tissue and primarily skeletal muscles) do not take up enough glucose in the bloodstream leading to persistent high blood glucose and possibly progression to diabetes. It is an appropriate short term trigger as a survival strategy to reroute available blood glucose exclusively to vital organs such as the brain, fetus, immune and circulatory systems in emergency conditions such as accidental/surgical traumas, infections and famine. This is why some patients who undergo surgery temporarily have high blood sugar which usually resolves once the acute condition is stabilized. However, lack of regular physical exercise can lead to excessive triggers of insulin resistance leading to type 2 diabetes.
Exercise and Glucose Uptake
Large amount of glucose is absorbed during meals but blood glucose concentration has to be within narrow limits in order to stay healthy. This is because abnormally high concentration of blood sugar is dangerous to blood vessels and other organs. Acute bout of exercise temporarily improves ability of insulin to drive glucose into the skeletal muscles which account for majority of glucose uptake.
Better still, repeated bouts of exercise, in form of regular physical activity, have additive effect beyond the short-lived insulin sensitivity of infrequent physical exercise and therefore reduce the risk of development of type 2 diabetes.
The brain almost exclusively relies on glucose for energy and has no capacity for storage. The skeletal muscles take up glucose and store about 80% as glycogen while the liver can store about 150g of glycogen, the largest percentage in term of its size. Glycogen is a readily mobilized storage form of glucose that can be broken down to yield glucose molecules when energy is needed. The skeletal muscles glycogen is stored for “in house” purposes as its broken down for energy as needed or stored for the next challenges of “fight or flight”. Conversely, the liver is sensitive to circulating blood glucose concentration and breaks down its stored glycogen to maintain concentration within normal limits. Both of these organs contribute to normal glucose concentration via efficient clearance in the bloodstream.
Muscular Contraction and Glucose Uptake in Cells
At the cellular level, the building block of skeletal muscle is a specialized muscle cell called myocyte. It is a typical animal cell that has the outer cell membrane to hold its internal contents. This membrane has on its surface insulin receptors where the insulin docks or perches on its cup-like surface in a “lock and key” or “hand in the glove” fashion. As insulin docks on these receptors during muscular contractions, it triggers a series of actions that cause the release of a secondary messenger called GLUT 4 transporter from inside the cell to the outer membrane. This secondary messenger immediately opens the “gates” on the membrane for glucose to flow passively into skeletal muscle cells. This accounts for substantial clearance of glucose in the circulatory system.
Insulin Resistance, Diabetes and Physical Inactivity
Skeletal muscle is the largest insulin sensitive organ but its sensitivity is largely dependent on muscle contractions. As noted above, it is not enough to have insulin receptors on the surface of muscle cell membrane; although, there has to be concomitant muscular contractions to propel the stored secondary messenger (GLUT 4 transporter) from inside the cell to the surface. Regular exercise therefore increases the amount of GLUT 4 transporter on cell surface and promotes the delivery of blood glucose to the cells. Engagement in physical exercise also reduces the glycogen content in skeletal muscles as it breaks down its stored “in house” glycogen into glucose for its energy needs and therefore promotes further glucose uptake from the bloodstream.
On the other hand, in spite of insulin presence, lack of regular activity reduces the number of secondary messenger (GLUT 4 transporter) on muscle cell surface and therefore decreases glucose uptake leading to insulin resistance. This is further compounded by what is called “cross talk” between organs. Reduce glucose uptake by skeletal muscles is signaled to the liver which in turn tries to compensate by dumping more glucose into the circulation. Chronic high blood glucose puts the pancreas, the organ that produces insulin, into overdrive to produce more insulin and this vicious cycle may eventually leads to overt diabetes.
Conclusion and Recommendations
A study reported an American randomized trial compromising of 3,234 people with insulin resistance to either treatment with metformin, a lifestyle adjustment that included dietary modification, and at least 2.5 hours of weekly physical exercise or placebo. Over a period of 2.8 years, the lifestyle modification reduced the risk of type 2 diabetes by 58% while the treatment with metformin only reduced the risk of diabetes by 31%.
The 2.5 hours of weekly exercise noted in the study is consistent with World Health Organization and American Guidelines on Physical Activity. It seems there is no credible excuse as 2.5 hours per week is far less than 19.6 hours a week of sitting in front of TV by average Americans. There are several other pathways where exercise improves, prevent or reverse diabetes which may be posted in future but the important take away is to engage the large muscles by regularly participating in leisure physical activity such as cycling, brisk walking, swimming or just about what is possible within any handicap conditions as everybody benefits from exercise.
Source :healthcrowonline.com
