The Rise and Fall of a Modern-Day Icarus

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By A Wilson

cover image of The Rise and Fall of a Modern-Day Icarus

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Written from a layman's perspective: some science involved. An attempt to understand the true nature of metabolic muscle mass increase—under the umbrella of bodybuilding—through the lens of metabolic typing. Why do most think that an increase of muscle mass leads to more resting fat metabolism? Consider carefully that the skeletal muscle fibres—which actually enlarge in size from mass training—are the Type IIb (Type IIx) fibres which are glycolytic, not lipolytic, in nature: pale under a microscope, these fibres contain little to no mitochondria. Mitochondria are thought to be the energy-factories inside the cell that house the lipolytic pathways known as Beta-oxidation and the Krebs cycle. Without mitochondria present, the only catabolic metabolic oxidation inside these pale white muscle fibres is cellular glycolytic metabolism—the catabolic oxidation of carbohydrates, in the form of glucose. Is it safe to assume that enlarging these fibres might result in the enlargement of an individual's overall level of carbohydrate metabolism and not his fat metabolism—as portrayed. Question: how would a carbohydrate-intensive, carbohydrate-ingesting, endogenous-insulin-releasing activity like bodybuilding—the expansion of such pale low-mitochondrial cells, glycolytic type IIb muscle fibres—increase fat-burning (lipolysis) significantly? Answer: it would not. Bodybuilding increases the metabolic stress on an individual by i) increasing the carbohydrate metabolism and ii) decreasing the fat metabolism, since endogenous insulin, released from dietary sources and required for muscle expansion, promotes glycogen deposition inside the muscle while at the same time suppressing fat metabolism. Increased metabolic stress is synonymous with an increasing level of energy defunctness. Increased glycogen deposition in the muscle expands the muscle, but the glucose required to build the glycogen comes from precious glucose energy reserves powering the rest of your body systems. If you are training for muscle size, but have a Stressor (a fast-oxidizer or protein- type) metabolism, and are aggressively eating more carbohydrates in order to release insulin to promote muscle size and glycogen deposition, you run the risk of developing "idiopathic" metabolic stress symptoms—including primary "idiopathic" hypertension—as you amplify your level of carbohydrate metabolism as a result of the enlargement of your muscle mass. If you are seriously lifting weights for size and eating a high carbohydrate diet—but have a Non-stressor (a slow-oxidizer or carbo-type) cellular metabolism—you will remain healthy as your musculature expands, but you too will incur a very small amount of metabolic stress increase. Read my personal life-quest as I fight to debunk the myth of muscle metabolism in order to understand the unexplored consequences of increased carbohydrate metabolism on individuals who are Slow-oxidizers versus Fast-oxidizers under a bodybuilding scenario. Download my free book today!

The Rise and Fall of a Modern-Day Icarus