A quantitative analysis of muscle cell changes in compensatory hypertrophy and work‐induced hypertrophy

Seiden, David L.

doi:10.1002/aja.1001450405

Cited by 49 publications

(39 citation statements)

References 23 publications

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“…It seems generally accepted that myonuclei are added under many hypertrophic conditions (Allen et al, 1995Bruusgaard et al, 2010;Cabric et al, 1987;Cabric and James, 1983;Cheek et al, 1971;Enesco and Puddy, 1964;Giddings and Gonyea, 1992;Kadi et al, 1999;Lipton and Schultz, 1979;McCall et al, 1998;Moss, 1968;Moss and Leblond, 1970;Roy et al, 1999;Schiaffino et al, 1976;Seiden, 1976;Winchester and Gonyea, 1992). However, the growth differs from the model shown in Fig.…”

Section: The Textbook Model For Muscle Size Regulationcontrasting

confidence: 39%

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Gundersen

2016

Journal of Experimental Biology

136

128

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Memory is a process in which information is encoded, stored, and retrieved. For vertebrates, the modern view has been that it occurs only in the brain. This review describes a cellular memory in skeletal muscle in which hypertrophy is 'remembered' such that a fibre that has previously been large, but subsequently lost its mass, can regain mass faster than naive fibres. A new cell biological model based on the literature, with the most reliable methods for identifying myonuclei, can explain this phenomenon. According to this model, previously untrained fibres recruit myonuclei from activated satellite cells before hypertrophic growth. Even if subsequently subjected to grave atrophy, the higher number of myonuclei is retained, and the myonuclei seem to be protected against the elevated apoptotic activity observed in atrophying muscle tissue. Fibres that have acquired a higher number of myonuclei grow faster when subjected to overload exercise, thus the nuclei represent a functionally important 'memory' of previous strength. This memory might be very long lasting in humans, as myonuclei are stable for at least 15 years and might even be permanent. However, myonuclei are harder to recruit in the elderly, and if the long-lasting muscle memory also exists in humans, one should consider early strength training as a public health advice. In addition, myonuclei are recruited during steroid use and encode a muscle memory, at least in rodents. Thus, extending the exclusion time for doping offenders should be considered.

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Section: The Textbook Model For Muscle Size Regulationcontrasting

confidence: 39%

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Gundersen

2016

Journal of Experimental Biology

136

128

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“…Changes in muscle fiber size are relative to changes in myonuclear number; myonuclear loss is associated with a reduction in muscle fiber size and, accordingly, growth of muscle fibers is associated with myonuclear addition (Seiden, 1976;Allen et al, 1995Allen et al, , 1999Mitchell and Pavlath, 2001). This finding is mirrored in our observations, where the mean muscle fiber size of the galectin-1 null mutant was decreased by ϳ22%, whereas the myonuclear number showed a reduction of ϳ24%, when compared with the respective wild-type values.…”

Section: Discussionmentioning

confidence: 99%

Lack of galectin‐1 results in defects in myoblast fusion and muscle regeneration

Georgiadis

Stewart

Pollard

et al. 2007

Developmental Dynamics

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Galectin-1 has been implicated in the development of skeletal muscle, being maximally expressed at the time of myofiber formation. Furthermore, in the presence of exogenous galectin-1, mononuclear myoblasts show increased fusion in vitro. In the current study, we have used the galectin-1 null mouse to elucidate the role of galectin-1 in skeletal muscle development and regeneration. Myoblasts derived from the galectin-1 mutant showed a reduced ability to fuse in vitro. In galectin-1 null mutants, there was evidence of a delay in muscle fiber development at the neonatal stage and muscle fiber diameter was reduced when compared with wild-type at the adult stage. Muscle regeneration was also compromised in the galectin-1 mutant with the process being delayed and a reduced fiber size being maintained. These results, therefore, show a definitive role for galectin-1 in fusion of myoblasts both in vitro, in vivo, and in regeneration after recovery from induced injury. Developmental Dynamics 236:1014 -1024, 2007.

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“…Embryonic myosin has been observed in regions remote from sites of focal injury leading to the suggestion that newly fused satellite cells, the myoblast-like cells in skeletal muscle (Mauro, 1961) that supply myofiber nuclei for muscle regeneration (Snow, 1977), might be responsible for altering myosin expression in these undamaged regions, as well as in sites of injury (Stewart et al, 1989). Satellite cells also supply hypertrophying fibers with additional nuclei (Schiaffino et al, 1972;Hanzlikova et al, 1975;Seiden, 1976;Snow, 1990;Winchester et al, 1991;Winchester and Gonyea, 19921, raising the possibility that satellite cells play a role in altering myosin isoform expression in hypertrophying fibers. We have examined this notion in the present study.…”

Section: Introductionmentioning

confidence: 99%

Role of satellite cells in altering myosin expression during avian skeletal muscle hypertrophy

McCormick

Schultz

1994

Developmental Dynamics

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This study examined whether satellite cells express an embryonic isoform of myosin upon fusion with hypertrophying muscle fibers. Anterior latissimus dorsi (ALD) muscle hypertrophy was induced in adult chickens by weighting one wing. One and 7 days of wingweighting produced significant increases in ALD muscle wet weight and in the number of mature fibers expressing ventricular-like embryonic (V-EMB) myosin. V-EMB myosin expression could be an event during regeneration of fibers injured by overload or part of the hypertrophy process itself. Although there was an increase in both the number of damaged fibers and the number of mature fibers expressing embryonic myosin after wingweighting, results from this study suggest that these two events were not necessarily related. The apparent health of fibers expressing V-EMB myosin and the lack of correlation between the numbers of damaged and V-EMB myosin positive fibers (r = 0.20) suggest that embryonic myosin expression in mature fibers was likely a feature of the hypertrophy process itself. The appearance of V-EMB myosin in mature fibers 1 day after wing weighting suggests that the change in myosin expression did not involve satellite cells since 24 hr is too short a time to permit more than limited satellite cell fusion. The relationship between satellite cells and embryonic myosin expression was examined more closely by labeling dividing satellite cells and their progeny with 5-bromo-2-deoxyuridine, and then colocalizing labeled myofiber nuclei and embryonic myosin in consecutive transverse sections of hypertrophied ALD muscle. One week of wingweighting resulted in marked increases in myofiber nuclear labeling index and myofiber nuclear density compared to contralatera1 control. V-EMB myosin was not expressed uniformly throughout individual fibers, but rather in discrete regions of varying length. Many V-EMB myosin positive regions had a higher labeled nuclear density than V-EMB myosin negative regions indicating that V-EMB myosin expression was associated with an accumulation of satellite cell progeny in a restricted area. However, it was also clear that satellite cell progeny were not the sole source of V-EMB myosin since labeled nuclei were completely absent from 41% of the V-EMB positive regions. Furthermore, the 0 1994 WILEY-LISS, INC.presence of new nuclei did not result in obligatory expression of embryonic myosin because many V-EMB negative regions had a high labeled nuclear density. Thus, recently incorporated nuclei arising by satellite cell division are implicated as one, but not the sole source of embryonic myosin in hypertrophying muscle. These observations suggest that the non-uniform pattern of embryonic myosin expression in hypertrophying muscle resulted from differences in nuclear activity, not necessarily the addition of new nuclei.

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A quantitative analysis of muscle cell changes in compensatory hypertrophy and work‐induced hypertrophy

Cited by 49 publications

References 23 publications

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Lack of galectin‐1 results in defects in myoblast fusion and muscle regeneration

Role of satellite cells in altering myosin expression during avian skeletal muscle hypertrophy

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