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Therefore, a more detailed and multifaceted analysis was required, including the rates of muscle contraction progression and relaxation in addition to torque rise time and half-relaxation time.
Taken together, these findings suggest that the muscle contraction progression was slowed down during SES, while it was maintained during SDSS.
These results are in line with the above-mentioned findings regarding muscle contraction progression, suggesting that muscle fatigue in terms of muscle contractile properties occurred during SES, whereas it was not the case during SDSS.
Muscular fatigue is characterized not only by loss of muscle force, but also by change of muscle contractile properties such as a slowing of the muscle contraction progression (Bigland-Ritchie et al. 1983).
To describe the muscle contraction progression and relaxation (Jones et al. 2006; Jones 2010; Bigland-Ritchie et al. 1983) during the fatiguing stimulation, we analyzed both ascending and descending phases of each muscle contraction.
In addition, we demonstrated that the spatially distributed sequential stimulation did not affect much the muscle contractile properties during the fatiguing stimulation, whereas single active electrode stimulation slowed down muscle contraction progression and relaxation.
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Treatment of PNDs with VGCC agonists after paralytic onset transiently potentiated nerve-elicited muscle contraction and delayed progression to neuromuscular failure.
Based on these results, we proposed a hypothesis to explain how the muscle contraction module affects DCM progression.
Our results also suggest that differences in vascular smooth muscle contraction influence the differential progression of PAD.
PP1 is an ubiquitous enzyme, regulating essential cellular processes such as cell cycle progression, protein synthesis, muscle contraction, carbohydrate metabolism, transcription, and neuronal signaling (reviewed in [79]).
These changes in the muscle contraction and organ morphogenesis modules may hold some clues to the progression of DCM.
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