Our current understanding on skeletal muscle hypertrophy is based on the hypothesis that increases in muscle mass are driven by an accumuation of myofibrillar proteins over time. That is, muscle protein synthesis (MPS) must exceed muscle protein breakdown (MPB), so the net result is an increase in myofibrillar protein mass. This hypothesis has a solid biological base and supporting scientific evidence. However, most studies on muscle hypertrophy use methods that are not able to assess myofibrillar hypertrophy directly; rather, they use methods that are considered a good proxy for it. Moreover, besides measuring skeletal muscle size at a single time point, they are not able to differentiate what is causing the changes in muscle size. For example, the size of a muscle can be increased temporarily by augmenting blood flow (“the pump”), which returns to baseline after a short time. Is this really hypertrophy?
In this article, I will elaborate on why it might be possible that what most short-term studies (4–16 weeks) are measuring is not necessarily myofibrillar hypertrophy, rather, fluid shifts. Thus, their interpretation towards long-term muscle gain and practical applications might have to be re-assessed.
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