Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle

Cory W. Baumann; Russell G. Rogers; Nidhi Gahlot; Christopher P. Ingalls

doi:10.14814/phy2.12081

Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle

Cory W. Baumann, Russell G. Rogers, Nidhi Gahlot, Christopher P. Ingalls

Research output: Contribution to journal › Article › peer-review

22 Scopus citations

Abstract

Strength deficits associated with eccentric contraction-induced muscle injury stem, in part, from impaired voltage-gated sarcoplasmic reticulum (SR) Ca2+ release. FKBP12 is a 12-kD immunophilin known to bind to the SR Ca2+ release channel (ryanodine receptor, RyR1) and plays an important role in excitation-contraction coupling. To assess the effects of eccentric contractions on FKBP12 content, we measured anterior crural muscle (tibialis anterior [TA], extensor digitorum longus [EDL], extensor hallucis longus muscles) strength and FKBP12 content in pellet and supernatant fractions after centrifugation via immunoblotting from mice before and after a single bout of either 150 eccentric or concentric contractions. There were no changes in peak isometric torque or FKBP12 content in TA muscles after concentric contractions. However, FKBP12 content was reduced in the pelleted fraction immediately after eccentric contractions, and increased in the soluble protein fraction 3 day after injury induction. FKBP12 content was correlated (P = 0.025; R² = 0.38) to strength deficits immediately after injury induction. In summary, eccentric contraction-induced muscle injury is associated with significant alterations in FKBP12 content after injury, and is correlated with changes in peak isometric torque.

Original language	English (US)
Article number	e12081
Journal	Physiological Reports
Volume	2
Issue number	7
DOIs	https://doi.org/10.14814/phy2.12081
State	Published - 2014
Externally published	Yes

Bibliographical note

Funding Information:
This work is supported by a grant from the National Institutes of HealthNIHAR-41802.

Funding Information:
This work is supported by a grant from the National Institutes of Health AR-41802.

Publisher Copyright:
© 2014 The Authors.

Keywords

Damage
Force
Mouse
Recovery
Skeletal muscle

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10.14814/phy2.12081

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title = "Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle",

abstract = "Strength deficits associated with eccentric contraction-induced muscle injury stem, in part, from impaired voltage-gated sarcoplasmic reticulum (SR) Ca2+ release. FKBP12 is a 12-kD immunophilin known to bind to the SR Ca2+ release channel (ryanodine receptor, RyR1) and plays an important role in excitation-contraction coupling. To assess the effects of eccentric contractions on FKBP12 content, we measured anterior crural muscle (tibialis anterior [TA], extensor digitorum longus [EDL], extensor hallucis longus muscles) strength and FKBP12 content in pellet and supernatant fractions after centrifugation via immunoblotting from mice before and after a single bout of either 150 eccentric or concentric contractions. There were no changes in peak isometric torque or FKBP12 content in TA muscles after concentric contractions. However, FKBP12 content was reduced in the pelleted fraction immediately after eccentric contractions, and increased in the soluble protein fraction 3 day after injury induction. FKBP12 content was correlated (P = 0.025; R2 = 0.38) to strength deficits immediately after injury induction. In summary, eccentric contraction-induced muscle injury is associated with significant alterations in FKBP12 content after injury, and is correlated with changes in peak isometric torque.",

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author = "Baumann, {Cory W.} and Rogers, {Russell G.} and Nidhi Gahlot and Ingalls, {Christopher P.}",

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AU - Rogers, Russell G.

AU - Gahlot, Nidhi

AU - Ingalls, Christopher P.

N1 - Funding Information: This work is supported by a grant from the National Institutes of HealthNIHAR-41802. Funding Information: This work is supported by a grant from the National Institutes of Health AR-41802. Publisher Copyright: © 2014 The Authors.

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N2 - Strength deficits associated with eccentric contraction-induced muscle injury stem, in part, from impaired voltage-gated sarcoplasmic reticulum (SR) Ca2+ release. FKBP12 is a 12-kD immunophilin known to bind to the SR Ca2+ release channel (ryanodine receptor, RyR1) and plays an important role in excitation-contraction coupling. To assess the effects of eccentric contractions on FKBP12 content, we measured anterior crural muscle (tibialis anterior [TA], extensor digitorum longus [EDL], extensor hallucis longus muscles) strength and FKBP12 content in pellet and supernatant fractions after centrifugation via immunoblotting from mice before and after a single bout of either 150 eccentric or concentric contractions. There were no changes in peak isometric torque or FKBP12 content in TA muscles after concentric contractions. However, FKBP12 content was reduced in the pelleted fraction immediately after eccentric contractions, and increased in the soluble protein fraction 3 day after injury induction. FKBP12 content was correlated (P = 0.025; R2 = 0.38) to strength deficits immediately after injury induction. In summary, eccentric contraction-induced muscle injury is associated with significant alterations in FKBP12 content after injury, and is correlated with changes in peak isometric torque.

AB - Strength deficits associated with eccentric contraction-induced muscle injury stem, in part, from impaired voltage-gated sarcoplasmic reticulum (SR) Ca2+ release. FKBP12 is a 12-kD immunophilin known to bind to the SR Ca2+ release channel (ryanodine receptor, RyR1) and plays an important role in excitation-contraction coupling. To assess the effects of eccentric contractions on FKBP12 content, we measured anterior crural muscle (tibialis anterior [TA], extensor digitorum longus [EDL], extensor hallucis longus muscles) strength and FKBP12 content in pellet and supernatant fractions after centrifugation via immunoblotting from mice before and after a single bout of either 150 eccentric or concentric contractions. There were no changes in peak isometric torque or FKBP12 content in TA muscles after concentric contractions. However, FKBP12 content was reduced in the pelleted fraction immediately after eccentric contractions, and increased in the soluble protein fraction 3 day after injury induction. FKBP12 content was correlated (P = 0.025; R2 = 0.38) to strength deficits immediately after injury induction. In summary, eccentric contraction-induced muscle injury is associated with significant alterations in FKBP12 content after injury, and is correlated with changes in peak isometric torque.

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KW - Force

KW - Mouse

KW - Recovery

KW - Skeletal muscle

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Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle

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