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December 30, 2011 at 10:59 am #319
PropaneFitnessKeymasterSo, we are de-sensitised to insulin in latter part of the day. We keep insulin low until lifting.After training we have GLY-4 translocation and the ability to absorb carbohydrate into muscle cells through non-insulin mediated transport. Therefore, why is there such an emphasis on insulin post-workout? Is it that insulin possesses additional anabolic properties?
December 31, 2011 at 12:20 am #15855
Naomi MostMemberSimply put, to maximize results from the workout. Insulin influences the ability of cells to uptake glucose, i.e. the presence of insulin makes glucose utilization happen in greater quantities.What we're doing with resistance training is manipulating the proteins in the muscle cells to give them the ability to uptake glucose in ways that insulin cannot touch.The result is an environment of excellent cell sensitivity to glucose (as well as a host of other good things, but let's just focus on the glucose here), as opposed to merely a "decent" response.
December 31, 2011 at 10:23 am #15856
PropaneFitnessGuestOk thanks. So what I think Im not understanding is that I understood insulin sensitivity to be determined by the positioning of the GLUT receptors in/on the cell. If the receptors are raised to the surface the cells are sensitive to insulin, if not they are resistant and require more insulin to cause more insulin to translocate to the surface? So with backloading, during the low carb/low insulin portion of the day GLUT receptors are sequestered in intracellular vesicles in muscle and fat cells - they become insulin resistant. We then stimulate GLUT4 translocation in muscle tissue through contraction - GLUT 4 raises to the surface and is therefore able to transport glucose into the cell via different mechanisms, the insulin spike enhances this and we get the optimal uptake of glucose into muscle tissue, hugely anabolic. However, wouldnt the large spike in insulin cause GLUT 4 to raise to the surface in fat cells as well? Is it simply that the marginal propensity is greater in muscle tissue as the GLUT 4 receptors are already at the surface and there is a "lag" so to speak with fat cells? Sorry for all the questions, just want to make sure I full understand.
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