Abstract

Traditionally it has been thought that muscle hypertrophy occurs primarily from an overload stimulus produced by progressively increasing an external load using at least 70% of one’s concentric one repetition maximum (1RM). Blood flow restricted exercise has been demonstrated to result in numerous positive training adaptions, specifically muscle hypertrophy and strength at intensities much lower than this recommendation. The mechanisms behind these adaptions are currently unknown but a commonly cited concept is that acute elevations of systemic hormones, specifically growth hormone (GH), play a large role with resistance training induced muscle hypertrophy, possibly through stimulating muscle protein synthesis (MPS). We hypothesize that the alterations in the intramuscular environment which results in the rapid recruitment of FT fibers, is the large driving force behind the skeletal muscle hypertrophy seen with blood flow restriction, whereas the external load and systemic endogenous hormone elevations may not be as important as once thought. It is further hypothesized that although skeletal muscle hypertrophy can be achieved at low intensities without blood flow restriction when taken to muscular failure, the overall volume of work required is much greater than that needed with blood flow restriction.

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