Book Excerpt: Carb Back-Loading

Exercise a Little Control

It probably sounds as though insulin sensitivity lies beyond our control. Muscles will, however, use sugar efficiently—in high-volume—without manipulating insulin sensitivity. Bypassing the whole sensitivity paradigm and moving tGLUT to the surface of cells is both possible and easy.

Any change in insulin sensitivity affects both fat cells and muscle tissue in the same way. If muscles become more sensitive to insulin and can store and use carbs, so can fat cells. If fat cells become less sensitive and find it difficult to use and store carbs, then so do muscles. The choices, then, are weak-and-ripped, or jacked-and-fat (or so it would seem). Of course, you can always just get fat, then spend 20-30 weeks leaning down as slowly as possible to see your hard-earned gains without losing anything.

Possessing the ability to translocate tGLUT at will changes everything. What is this magical power of which I speak? It’s resistance training. I don’t expect this to be a massive revelation. Resistance training triggers so many cellular reactions within muscle that it seems reasonable that it can also replace some of insulin’s functionality. How, then, can we benefit from the translocation of tGLUT without insulin playing a role?

This is where those studies on diabetic patients have paid off—initiating my autodidactic endeavor into the GLUT and other cellular transport systems. I happened upon a paper that tested insulin sensitivity and glucose clearance in type II diabetics after resistance training[1]. Despite a lack of increase in insulin sensitivity immediately post-exercise, glucose clearance from the bloodstream increased. This seemed counterintuitive until I learned about the insulin-independent translocation of tGLUT[2].

Non-insulin mediated translocation of tGLUT occurs with resistance training in all mammals, diabetic or otherwise[3]. Resistance training prepares muscles to soak up sugar even before insulin is present. The moment sugar hits the bloodstream, skeletal muscle doesn’t need to wait for a rise in insulin to absorb glucose. This pre-insulin clearance of carbs can decrease the insulin response, and it robs fat cells of both a large insulin spike and all that precious sugar they’d just love to convert to fat.

For diabetics, this process is both extraordinary and life-altering. It doesn’t matter that a type II diabetic’s cells don’t react to insulin any longer, because resistance training mimics a key function of insulin. With resistance training, a diabetic can clear sugar from the bloodstream without medication, while fat cells remain insulin-resistant.

I want to be very clear here: This process operates independently of insulin. When talking about non-insulin-mediated translocation (note the ‘non’), we can ignore insulin, at least as far as its necessity for increasing glucose absorption and speeding recovery from training. Recovery and resynthesis of glycogen stores depends on carbohydrate availability—and not necessarily on insulin secretion (although insulin may serve other purposes in the process of muscle growth).

squatDon’t confuse these concepts. Translocation of tGLUT caused by muscular contractions does not increase insulin sensitivity. The two are unrelated. Essentially, resistance training achieves results similar to those initiated by insulin, but without it. It may sound redundant, but there’s a lot of confusion about this topic, and choosing proper post-training nutrition to amplify and attenuate the right signals depends on understanding this fact.

NOTE: The translocation of tGLUT that occurs with exercise is not related to insulin function or increased insulin sensitivity. tGLUT move to the surface of muscle cells when contracting under a load. This process is called insulin-independent translocation.

This is an amazing process, and it exemplifies the concept of MTR—targeting a response that normally affects multiple tissues exclusively in one type of tissue. We choose which tissue absorbs carbs without increasing another tissue’s absorption—despite the fact that, in other cases, the ability of both to use carbs rises and falls together. Resistance training decouples the two.

As an added advantage, resistance training triggers two more desirable changes. Resistance training causes tGLUT to move around without insulin, but it also increases the amount and concentration of tGLUT in muscle cells[4]. In other words, tGLUT activate with training, and there’s also more of them to activate. Resistance training equips muscle cells to absorb sugar at a faster rate, either for storage or energy production.

Along with that, muscle cells also become more sensitive to insulin over time, so when things calm down after training and everything goes back to normal, your muscle cells react faster and more powerfully to insulin than your fat cells can—once again clearing glucose from circulation before fat cells can get hold of it and turn it into fat.

This is just a small sampling of the biomolecular changes that occur within muscle cells with resistance training. Covering all these changes, and their effects on health, well-being, strength, and fat loss would fill its own volume. For now, however, the focus is on the changes that deal with GLUT and insulin.

For diabetics, the benefit is clear: Instead of medication that makes both muscle and fat cells sensitive to insulin again—allowing them to get fatter and sicker—it’s possible to lift weights and get healthy. What kind of nonsense am I talking here? Sure, it’d be far easier to just pop a pill and get fatter. Maybe the real benefit here will be seen by you: The person who already trains hard, battles with the iron on a daily basis, and strives for more than just heath. This is for those of you who want to be exceptional.