Eccentric exercise markedly increases c-Jun NH2-terminal kinase activity in human skeletal muscle

Marni D. Boppart, Doron Aronson, Lindsay Gibson, Ronenn Roubenoff, Leslie W. Abad, Jonathan Bean, Laurie J. Goodyear, Roger A. Fielding

Research output: Contribution to journalArticlepeer-review

Abstract

Eccentric contractions require the lengthening of skeletal muscle during force production and result in acute and prolonged muscle injury. Because a variety of stressors, including physical exercise and injury, can result in the activation of the c-Jun NH2-terminal kinase (JNK) intracellular signaling cascade in skeletal muscle, we investigated the effects of eccentric exercise on the activation of this stress-activated protein kinase in human skeletal muscle. Twelve healthy subjects (7 men, 5 women) completed maximal concentric or eccentric knee extensions on a KinCom isokinetic dynamometer (10 sets, 10 repetitions). Percutaneous needle biopsies were obtained from the vastus lateralis muscle 24 h before exercise (basal), immediately postexercise, and 6 h postexercise. Whereas both forms of exercise increased JNK activity immediately postexercise, eccentric contractions resulted in a much higher activation (15.4 ± 4.5 vs. 3.5 ± 1.4-fold increase above basal, eccentric vs. concentric). By 6 h after exercise, JNK activity decreased back to baseline values. In contrast to the greater activation of JNK with eccentric exercise, the mitogen-activated protein kinase kinase 4, the immediate upstream regulator of JNK, was similarly activated by concentric and eccentric exercise. Because the activation of JNK promotes the phosphorylation of a variety of transcription factors, including c-Jun, the results from this study suggest that JNK may be involved in the molecular and cellular adaptations that occur in response to injury-producing exercise in human skeletal muscle.

Original languageEnglish (US)
Pages (from-to)1668-1673
Number of pages6
JournalJournal of Applied Physiology
Volume87
Issue number5
DOIs
StatePublished - Nov 1999

Keywords

  • Injury
  • Interleukin-6
  • Mitogen-activated protein kinase kinase 4

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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