Coordinated alpha-crystallin B phosphorylation and desmin expression indicate adaptation and deadaptation to resistance exercise-induced loading in human skeletal muscle

Research output: Contribution to journalArticleResearchpeer review

Authors

  • Daniel Jacko
  • Käthe Bersiner
  • Oliver Schulz
  • Axel Przyklenk
  • Fabian Spahiu
  • Jörg Höhfeld
  • Wilhelm Bloch
  • Sebastian Gehlert

External Research Organisations

  • German Sport University Cologne
  • Olympiastützpunkt NRW/Rheinland
  • University of Hildesheim
  • University of Bonn
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Details

Original languageEnglish
Pages (from-to)C300-C312
JournalAmerican Journal of Physiology - Cell Physiology
Volume319
Issue number2
Publication statusPublished - 8 Jan 2020
Externally publishedYes

Abstract

Skeletal muscle is a target of contraction-induced loading (CiL), leading to protein unfolding or cellular perturbations, respectively. While cytoskeletal desmin is responsible for ongoing structural stabilization, in the immediate response to CiL, alpha-crystallin B (CRYAB) is phosphorylated at serine 59 ( pCRYAB S59) by P38, acutely protecting the cytoskeleton. To reveal adaptation and deadaptation of these myofibrillar subsystems to CiL, we examined CRYAB, P38, and desmin regulation following resistance exercise at diverse time points of a chronic training period. Mechanosensitive JNK phosphorylation ( pJNK T183/ Y185) was determined to indicate the presence of mechanical components in CiL. Within 6 wk, subjects performed 13 resistance exercise bouts at the 8–12 repetition maximum, followed by 10 days detraining and a final 14th bout. Biopsies were taken at baseline and after the 1st, 3rd, 7th, 10th, 13th, and 14th bout. To assess whether potential desensitization to CiL can be mitigated, one group trained with progressive and a second with constant loading. As no group differences were found, all subjects were combined for statistics. Total and phosphorylated P38 was not regulated over the time course. pCRYAB S59 and pJNK T183/Y185 strongly increased following the unaccustomed first bout. This exercise-induced pCRYAB S59/ pJNK T183/Y185 increase disappeared with the 10th until 13th bout. As response to the detraining period, the 14th bout led to a renewed increase in pCRYAB S59. Desmin content followed pCRYAB S59 inversely, i.e., was up- when pCRYAB S59 was downregulated and vice versa. In conclusion, the pCRYAB S59 response indicates increase and decrease in resistance to CiL, in which a reinforced desmin network could play an essential role by structurally stabilizing the cells.

Keywords

    CRYAB, Desmin, Mechanical stress, Muscle, Resistance exercise

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Physiology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology

Cite this

Coordinated alpha-crystallin B phosphorylation and desmin expression indicate adaptation and deadaptation to resistance exercise-induced loading in human skeletal muscle. / Jacko, Daniel; Bersiner, Käthe; Schulz, Oliver et al.
In: American Journal of Physiology - Cell Physiology, Vol. 319, No. 2, 08.01.2020, p. C300-C312.

Research output: Contribution to journalArticleResearchpeer review

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title = "Coordinated alpha-crystallin B phosphorylation and desmin expression indicate adaptation and deadaptation to resistance exercise-induced loading in human skeletal muscle",
abstract = "Skeletal muscle is a target of contraction-induced loading (CiL), leading to protein unfolding or cellular perturbations, respectively. While cytoskeletal desmin is responsible for ongoing structural stabilization, in the immediate response to CiL, alpha-crystallin B (CRYAB) is phosphorylated at serine 59 ( pCRYAB S59) by P38, acutely protecting the cytoskeleton. To reveal adaptation and deadaptation of these myofibrillar subsystems to CiL, we examined CRYAB, P38, and desmin regulation following resistance exercise at diverse time points of a chronic training period. Mechanosensitive JNK phosphorylation ( pJNK T183/ Y185) was determined to indicate the presence of mechanical components in CiL. Within 6 wk, subjects performed 13 resistance exercise bouts at the 8–12 repetition maximum, followed by 10 days detraining and a final 14th bout. Biopsies were taken at baseline and after the 1st, 3rd, 7th, 10th, 13th, and 14th bout. To assess whether potential desensitization to CiL can be mitigated, one group trained with progressive and a second with constant loading. As no group differences were found, all subjects were combined for statistics. Total and phosphorylated P38 was not regulated over the time course. pCRYAB S59 and pJNK T183/Y185 strongly increased following the unaccustomed first bout. This exercise-induced pCRYAB S59/ pJNK T183/Y185 increase disappeared with the 10th until 13th bout. As response to the detraining period, the 14th bout led to a renewed increase in pCRYAB S59. Desmin content followed pCRYAB S59 inversely, i.e., was up- when pCRYAB S59 was downregulated and vice versa. In conclusion, the pCRYAB S59 response indicates increase and decrease in resistance to CiL, in which a reinforced desmin network could play an essential role by structurally stabilizing the cells.",
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TY - JOUR

T1 - Coordinated alpha-crystallin B phosphorylation and desmin expression indicate adaptation and deadaptation to resistance exercise-induced loading in human skeletal muscle

AU - Jacko, Daniel

AU - Bersiner, Käthe

AU - Schulz, Oliver

AU - Przyklenk, Axel

AU - Spahiu, Fabian

AU - Höhfeld, Jörg

AU - Bloch, Wilhelm

AU - Gehlert, Sebastian

N1 - Publisher Copyright: Copyright © 2020 the American Physiological Society

PY - 2020/1/8

Y1 - 2020/1/8

N2 - Skeletal muscle is a target of contraction-induced loading (CiL), leading to protein unfolding or cellular perturbations, respectively. While cytoskeletal desmin is responsible for ongoing structural stabilization, in the immediate response to CiL, alpha-crystallin B (CRYAB) is phosphorylated at serine 59 ( pCRYAB S59) by P38, acutely protecting the cytoskeleton. To reveal adaptation and deadaptation of these myofibrillar subsystems to CiL, we examined CRYAB, P38, and desmin regulation following resistance exercise at diverse time points of a chronic training period. Mechanosensitive JNK phosphorylation ( pJNK T183/ Y185) was determined to indicate the presence of mechanical components in CiL. Within 6 wk, subjects performed 13 resistance exercise bouts at the 8–12 repetition maximum, followed by 10 days detraining and a final 14th bout. Biopsies were taken at baseline and after the 1st, 3rd, 7th, 10th, 13th, and 14th bout. To assess whether potential desensitization to CiL can be mitigated, one group trained with progressive and a second with constant loading. As no group differences were found, all subjects were combined for statistics. Total and phosphorylated P38 was not regulated over the time course. pCRYAB S59 and pJNK T183/Y185 strongly increased following the unaccustomed first bout. This exercise-induced pCRYAB S59/ pJNK T183/Y185 increase disappeared with the 10th until 13th bout. As response to the detraining period, the 14th bout led to a renewed increase in pCRYAB S59. Desmin content followed pCRYAB S59 inversely, i.e., was up- when pCRYAB S59 was downregulated and vice versa. In conclusion, the pCRYAB S59 response indicates increase and decrease in resistance to CiL, in which a reinforced desmin network could play an essential role by structurally stabilizing the cells.

AB - Skeletal muscle is a target of contraction-induced loading (CiL), leading to protein unfolding or cellular perturbations, respectively. While cytoskeletal desmin is responsible for ongoing structural stabilization, in the immediate response to CiL, alpha-crystallin B (CRYAB) is phosphorylated at serine 59 ( pCRYAB S59) by P38, acutely protecting the cytoskeleton. To reveal adaptation and deadaptation of these myofibrillar subsystems to CiL, we examined CRYAB, P38, and desmin regulation following resistance exercise at diverse time points of a chronic training period. Mechanosensitive JNK phosphorylation ( pJNK T183/ Y185) was determined to indicate the presence of mechanical components in CiL. Within 6 wk, subjects performed 13 resistance exercise bouts at the 8–12 repetition maximum, followed by 10 days detraining and a final 14th bout. Biopsies were taken at baseline and after the 1st, 3rd, 7th, 10th, 13th, and 14th bout. To assess whether potential desensitization to CiL can be mitigated, one group trained with progressive and a second with constant loading. As no group differences were found, all subjects were combined for statistics. Total and phosphorylated P38 was not regulated over the time course. pCRYAB S59 and pJNK T183/Y185 strongly increased following the unaccustomed first bout. This exercise-induced pCRYAB S59/ pJNK T183/Y185 increase disappeared with the 10th until 13th bout. As response to the detraining period, the 14th bout led to a renewed increase in pCRYAB S59. Desmin content followed pCRYAB S59 inversely, i.e., was up- when pCRYAB S59 was downregulated and vice versa. In conclusion, the pCRYAB S59 response indicates increase and decrease in resistance to CiL, in which a reinforced desmin network could play an essential role by structurally stabilizing the cells.

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KW - Desmin

KW - Mechanical stress

KW - Muscle

KW - Resistance exercise

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U2 - DOI: 10.1152/ajpcell.00087.2020

DO - DOI: 10.1152/ajpcell.00087.2020

M3 - Article

VL - 319

SP - C300-C312

JO - American Journal of Physiology - Cell Physiology

JF - American Journal of Physiology - Cell Physiology

SN - 0363-6143

IS - 2

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