*** Significantly different compared with 2 and 4 weeks, P < .05. **Significantly different compared with pre and 2 weeks, P < .05. *Significantly different compared with pre, P < .05. A significant group × time interaction was observed for myonuclear content ( P < .05) as well as myonuclear domain ( P < .05), resulting in separate one‐way repeated measures ANOVAs and pairwise comparisons being performed to identify within‐group effects. Data were analysed with a two‐way repeated measures ANOVA with time (pre, 2, 4, 8 and 12 weeks) as within subject factor and group (Small vs Large) as between subject factor. Muscle satellite cells were identified by NCAM staining and excluded from the myonuclear counts. Myonuclear content and fibre size were determined by immunofluorescent microscopy as described previously. At least 100 type I and 100 type II muscle fibres per subject were included to make a reliable estimation of myonuclear contentĬhanges in myonuclear domain size (A), myonuclear content (B) and muscle fibre size (C) in response to 2, 4, 8 and 12 weeks of progressive resistance exercise training in healthy young men with a relatively small (2000 µm 2 Large group Large group n = 10) myonuclear domain size at baseline. Muscle satellite cells were identified by Pax7 or NCAM staining and excluded from the myonuclear counts. A Dapi + cell was considered to be a myonucleus when at least 50% of the staining was present within the muscle fibre identified by laminin staining. Staining included antibodies for laminin (cell border), MHCI (type I muscle fibres), Dapi (nuclei), Pax7 or NCAM (satellite cells). Muscle fibre size and myonuclear content were determined by immunofluorescent microscopy of muscle cross‐sections. All samples were collected with subjects at rest following an overnight fast. Acta Physiologica published by John Wiley & Sons Ltd on behalf of Scandinavian Physiological Society.Ĭorrelation analysis between type I and type II muscle fibre size and number of myonuclei per fibre (A and B linear relation) and myonuclear domain size (C and D logarithmic relation) in percutaneous biopsy samples taken from the vastus lateralis of both healthy adult men (n = 330) and women (n = 88). Muscle adaptation muscle memory myonuclear domain size myonuclei satellite cell. Finally, suggestions for future research are provided to establish whether muscle memory really exists in humans. Furthermore, to provide additional insight in the potential presence of muscle memory by myonuclear permanence in humans, we present new data on previously performed exercise training studies. The goal of the present review was to discuss the evidence for the existence of "muscle memory" in both animal and human models of muscle fibre hypertrophy as well as atrophy. Nevertheless, there are several studies in humans that provide evidence to potentially support or contradict (parts of) the muscle memory hypothesis. Whether the postulated mechanism also holds true in humans remains largely ambiguous. Such myonuclear permanence has been suggested to constitute a mechanism allowing the muscle fibre to (re)grow more efficiently during retraining, a phenomenon referred to as "muscle memory." The concept of "muscle memory by myonuclear permanence" has mainly been based on data attained from rodent experimental models. However, data from recent animal studies suggest that myonuclei that are added to support muscle fibre hypertrophy are not lost within various muscle atrophy models. The myonuclear domain is kept (relatively) constant by adding additional nuclei (supplied by muscle satellite cells) during muscle fibre hypertrophy and nuclear loss (by apoptosis) during muscle fibre atrophy. Within the current paradigm of the myonuclear domain theory, it is postulated that a linear relationship exists between muscle fibre size and myonuclear content.
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