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Skeletal Muscles Do Not Undergo Apoptosis During Either Atrophy or Programmed Cell Death-Revisiting the Myonuclear Domain Hypothesis

PainSci » bibliography » Schwartz 2018
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Tags: biology, strength, neat, good news, exercise, self-treatment, treatment

Two articles on PainSci cite Schwartz 2018: 1. Strength Training for Pain & Injury Rehab2. Strength Training Frequency

PainSci commentary on Schwartz 2018: ?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

Why is it easier to get back in shape than it is to get into shape in the first place? Some adaptations to muscle training are temporary and vanish quickly if you don't keep working out. But others, like the addition of extra muscle nuclei, appear to be more or less permanent. Nuclei are added as you train so that they can build and manage more proteins in a plumper muscle cell. When you stop training, the cell slowly deflates — atrophies — but the nuclei helpfully remain, dormant, waiting until you are ready to exercise again. See Alex Hutchinson’s more detailed analysis of the study.

~ Paul Ingraham

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Skeletal muscles are the largest cells in the body and are one of the few syncytial ones. There is a longstanding belief that a given nucleus controls a defined volume of cytoplasm, so when a muscle grows (hypertrophy) or shrinks (atrophy), the number of myonuclei change accordingly. This phenomenon is known as the "myonuclear domain hypothesis." There is a general agreement that hypertrophy is accompanied by the addition of new nuclei from stem cells to help the muscles meet the enhanced synthetic demands of a larger cell. However, there is a considerable controversy regarding the fate of pre-existing nuclei during atrophy. Many researchers have reported that atrophy is accompanied by the dramatic loss of myonuclei via apoptosis. However, since there are many different non-muscle cell populations that reside within the tissue, these experiments cannot easily distinguish true myonuclei from those of neighboring mononuclear cells. Recently, two independent models, one from rodents and the other from insects, have demonstrated that nuclei are not lost from skeletal muscle fibers when they undergo either atrophy or programmed cell death. These and other data argue against the current interpretation of the myonuclear domain hypothesis and suggest that once a nucleus has been acquired by a muscle fiber it persists.

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