Muscle memory: virtues of your youth?

Gundersen, Kristian; Bruusgaard, Jo C.; Egner, Ingrid M.; Eftestøl, Einar; Bengtsen, Mads

doi:10.1113/jp276354

Cited by 19 publications

(24 citation statements)

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“…Consistent with the decrease in fibre CSA following denervation, the ratio fibre CSA per nuclear profile was 12%‐14% smaller at both 10 and 30 dpc (Figure C) . These results are consistent with recent reports evidencing that both fibre atrophy caused by denervation, nerve impulse bloc (see also below) or unloading, and fibre growth caused by loading or re‐training can occur without significant net change of myonuclei density see however also …”

Section: Discussionsupporting

confidence: 91%

“…72,73 These results are consistent with recent reports evidencing that both fibre atrophy caused by denervation, nerve impulse bloc (see also below) or unloading, and fibre growth caused by loading or re-training can occur without significant net change of myonuclei density 74,75 see however also. 39,[76][77][78] In this study, we also recorded an increased occurrence of myonuclei with a central position, a change that became significant at 30 dpc ( Figures 3D and 4A). Such nuclei are believed to be newly incorporated into the fibre and to derive from the SC niche (see Introduction) suggesting an accretion of myonuclei during the re-growth of the fibres once they became re-innervated (10-14 dpc) which matches the concurrent increase in MDF and NumbL mRNAs (see below).…”

Section: Discussionsupporting

confidence: 63%

“…However, we cannot provide evidence for the origin of these central nuclei since our experimental design did not include tissue labelling of markers for SCs or differentiating myoblasts, still our data would be consistent with a small flux of myonuclei through the sequential atrophy and re-growth processes following nerve crush. This issue certainly deserves further attention (see also below) especially in the light of recent observations evidencing that genetic reduction/ablation of the SC pool in adult (>4-month-old) mice does not prevent myofibre growth in response to loading or myofibre re-growth following atrophy in adult animals (>4 month old) 79-81 see however 39,76 ; reviewed in. 38,82 Complementary to the nerve crush model used here is chronic denervation where re-innervation is prevented 74,83,84 and tertrotoxin blockage of axon impulses (TTX; 74,[83][84][85][86][87] ).…”

Section: Discussionmentioning

confidence: 99%

“…[28][29][30] The signalling pathways governing contractile protein breakdown is normally active and balanced by stimuli to increase myosins to enlarge myofibre size and muscle mass. [30][31][32][33][34][35][36] Originating from theory that the DNA of a nucleus can support but a limited cellular volume and that this relationship sets a ceiling for growth (37)(38)(39) ; myonuclear domain, MND), major alteration in fibre size should be accompanied by either a reduction of total number of myonuclei or the recruitment and incorporation of de novo formed myonuclei deriving from the regional stem cell niche, ie, Satellite cell (SC) niche. [40][41][42][43][44] As currently debated, more recent data suggest that both significant atrophy and hypertrophy can occur without changes to number of myonuclei 39,41 or replenishment of myonuclei from the SC cell niche.…”

mentioning

confidence: 99%

“…[30][31][32][33][34][35][36] Originating from theory that the DNA of a nucleus can support but a limited cellular volume and that this relationship sets a ceiling for growth (37)(38)(39) ; myonuclear domain, MND), major alteration in fibre size should be accompanied by either a reduction of total number of myonuclei or the recruitment and incorporation of de novo formed myonuclei deriving from the regional stem cell niche, ie, Satellite cell (SC) niche. [40][41][42][43][44] As currently debated, more recent data suggest that both significant atrophy and hypertrophy can occur without changes to number of myonuclei 39,41 or replenishment of myonuclei from the SC cell niche. 38,40 Evidence provided (see references above) suggest that skeletal muscle atrophy associated with chronic systemic diseases and/or ageing are instigated by alteration in the balance of atrophy and hypertrophy stimuli and/ or dysfunction of the replenishment of myonuclei from the satellite cell niche and/or disturbed innervation.…”

mentioning

confidence: 99%

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Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush

et al. 2019

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Aim To resolve timing and coordination of denervation atrophy and the re‐innervation recovery process to discern correlations indicative of common programs governing these processes. Methods Female Sprague‐Dawley (SD) rats had a unilateral sciatic nerve crush. Based on longitudinal behavioural observations, the triceps surae muscle was analysed at different time points post‐lesion. Results Crush results in a loss of muscle function and mass (−30%) followed by a recovery to almost pre‐lesion status at 30 days post‐crush (dpc). There was no loss of fibres nor any significant change in the number of nuclei per fibre but a shift in fibres expressing myosins I and II that reverted back to control levels at 30 dpc. A residual was the persistence of hybrid fibres. Early on a CHNR ‐ε to ‐γ switch and a re‐expression of embryonic MyHC showed as signs of denervation. Foxo1, Smad3, Fbxo32 and Trim63 transcripts were upregulated but not Myostatin, InhibinA and ActivinR2B. Combined this suggests that the mechanism instigating atrophy provides a selectivity of pathway(s) activated. The myogenic differentiation factors (MDFs: Myog, Myod1 and Myf6) were upregulated early on suggesting a role also in the initial atrophy. The regulation of these transcripts returned towards baseline at 30 dpc. The examined genes showed a strong baseline covariance in transcript levels which dissolved in the response to crush driven mainly by the MDFs. At 30 dpc the naïve expression pattern was re‐established. Conclusion Peripheral nerve crush offers an excellent model to assess and interfere with muscle adaptions to denervation and re‐innervation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush

et al. 2019

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Enhanced skeletal muscle contractile function and corticospinal excitability precede strength and architectural adaptations during lower-limb resistance training

et al. 2023

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Purpose Evolving investigative techniques are providing greater understanding about the early neuromuscular responses to resistance training among novice exercisers. The aim of this study was to investigate the time-course of changes in muscle contractile mechanics, architecture, neuromuscular, and strength adaptation during the first 6-weeks of lower-limb resistance training. Methods Forty participants: 22 intervention (10 males/12 females; 173.48 ± 5.20 cm; 74.01 ± 13.13 kg) completed 6-week resistance training, and 18 control (10 males/8 females; 175.52 ± 7.64 cm; 70.92 ± 12.73 kg) performed no resistance training and maintained their habitual activity. Radial muscle displacement (Dm) assessed via tensiomyography, knee extension maximal voluntary contraction (MVC), voluntary activation (VA), corticospinal excitability and inhibition via transcranial magnetic stimulation, motor unit (MU) firing rate, and muscle thickness and pennation angle via ultrasonography were assessed before and after 2, 4, and 6-weeks of dynamic lower-limb resistance training or control. Results After 2-weeks training, Dm reduced by 19–25% in the intervention group; this was before any changes in neural or morphological measures. After 4-weeks training, MVC increased by 15% along with corticospinal excitability by 16%; however, there was no change in VA, corticospinal inhibition, or MU firing rate. After 6-weeks training there was further MVC increase by 6% along with muscle thickness by 13–16% and pennation angle by 13–14%. Conclusion Enhanced contractile properties and corticospinal excitability occurred before any muscle architecture, neural, and strength adaptation. Later increases in muscular strength can be accounted for by architectural adaptation.

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2023

Principles of Cognitive Rehabilitation

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Muscle memory: virtues of your youth?

Cited by 19 publications

References 9 publications

Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush

Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush

Enhanced skeletal muscle contractile function and corticospinal excitability precede strength and architectural adaptations during lower-limb resistance training

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