Abstract
Prevailing theories of hypertrophy assert that it is a form
of overcompensation in response to microtrauma induced by mechanical loading. There is undoubtedly some degree of soft tissue remodeling in accordance with
Davis’ law, but no degree of physiological cross-sectional area augmentation
can adequately explain the extreme degree of hypertrophy observed in many
strength and physique athletes. Increases in muscle mass without correlating
increases in contractile force are attributed to sarcoplasmic hypertrophy; a
proliferation of sarcoplasm in response to chronic deficiencies in localized
glycogen stores induced by anaerobic training. The functionally superfluous
muscle mass exhibited by the aforementioned athletes can indeed be attributed
to a glycogen-mediated increase in cell volume, but the process by which this
occurs has been misinterpreted as a relative function of soft tissue
restructuring. The widely accepted hypotheses of cellular alteration as a
response to mechanical stress and/or imposed energy demands implies the
existence of a uniquely maladaptive and redundant evolutionary trait suited
more to modern aesthetics than Pleistocene survival. It is far more likely that
structural adaptations of individual myocytes serve to facilitate acid-base
homeostasis, which is threatened by intracellular hydrogen ions liberated via
glycolysis. Intracellular alkalization via lactate dehydrogenase is subject to
feedback inhibition, which consigns the rate of glycolysis to the efficiency of
monocarboxylate transporters. All measures of anaerobic efficiency, to include
glycogen storage and utilization, are manifestly dependent on the modulation of
transporter proteins. This research aims to demonstrate that muscular hypertrophy
is the collateral result of survival-based structural modifications, and
therefore only tangentially related to conventional loading-based training
protocols.
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