Intramuscular Contributions to Low-Frequency Force Potentiation Induced by a High-Frequency Conditioning Stimulation.

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_25ECEF998E44
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Intramuscular Contributions to Low-Frequency Force Potentiation Induced by a High-Frequency Conditioning Stimulation.
Périodique
Frontiers in physiology
Auteur(s)
Cheng A.J., Neyroud D., Kayser B., Westerblad H., Place N.
ISSN
1664-042X (Print)
ISSN-L
1664-042X
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
8
Pages
712
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Electrically-evoked low-frequency (submaximal) force is increased immediately following high-frequency stimulation in human skeletal muscle. Although central mechanisms have been suggested to be the major cause of this low-frequency force potentiation, intramuscular factors might contribute. Thus, we hypothesized that two intramuscular Ca2+-dependent mechanisms can contribute to the low-frequency force potentiation: increased sarcoplasmic reticulum Ca2+ release and increased myofibrillar Ca2+ sensitivity. Experiments in humans were performed on the plantar flexor muscles at a shortened, intermediate, and long muscle length and electrically evoked contractile force and membrane excitability (i.e., M-wave amplitude) were recorded during a stimulation protocol. Low-frequency force potentiation was assessed by stimulating with a low-frequency tetanus (25 Hz, 2 s duration), followed by a high-frequency tetanus (100 Hz, 2 s duration), and finally followed by another low-frequency (25 Hz, 2 s duration) tetanus. Similar stimulation protocols were performed on intact mouse single fibers from flexor digitorum brevis muscle, whereby force and myoplasmic free [Ca2+] ([Ca2+]i) were assessed. Our data show a low-frequency force potentiation that was not muscle length-dependent in human muscle and it was not accompanied by any increase in M-wave amplitude. A length-independent low-frequency force potentiation could be replicated in mouse single fibers, supporting an intramuscular mechanism. We show that at physiological temperature (31°C) this low-frequency force potentiation in mouse fibers corresponded with an increase in sarcoplasmic reticulum (SR) Ca2+ release. When mimicking the slower contractile properties of human muscle by cooling mouse single fibers to 18°C, the low-frequency force potentiation was accompanied by minimally increased SR Ca2+ release and hence it could be explained by increased myofibrillar Ca2+ sensitivity. Finally, introducing a brief 200 ms pause between the high- and low-frequency tetanus in human and mouse muscle revealed that the low-frequency force potentiation is abolished, arguing that increased myofibrillar Ca2+ sensitivity is the main intramuscular mechanism underlying the low-frequency force potentiation in humans.

Mots-clé
M-wave, intact single fiber, intracellular Ca2+, muscle length, plantar flexors
Pubmed
Web of science
Open Access
Oui
Création de la notice
08/01/2018 13:07
Dernière modification de la notice
21/08/2019 7:08
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