Elevation of myostatin and FOXOs in prolonged muscular impairment induced by eccentric contractions in rat medial gastrocnemius muscle

Eisuke Ochi, Tatsuro Hirose, Kenji Hiranuma, Seok Ki Min, Naokata Ishii, Koichi Nakazato

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

This study aimed to investigate torque deficit and activation of protein synthesis and/or protein degradation signaling pathways during the early and recovery phase after high- and low-velocity eccentric contractions (ECs). Male Wistar rats (n = 36) were randomly divided into fast angular velocity ECs group (FAST; 180°/s; n = 12), slow ECs group (SLOW; 30°/s; n = 12), and control group (control; n =12). ECs comprised four sets of five forced dorsiflexions combined with electrical stimulation of the plantar flexors. Isometric tetanic torque was measured before and after ECs. Tissue contents of Akt(P) (P, phosphorylated), mammalian target of rapamycin (mTOR)(P), 70-kDa ribosomal protein S6 kinase (P70S6k), P70S6k(P), forkhead transcription factor 1 of the O class (FOXOl), FOXOl(P), FOXO3, FOXO3(P), myostatin, and activin receptor type IIB (ActRIIB) were measured. The isometric tetanic torque after ECs was significantly lower in FAST than in SLOW (days 1, 3, and 5, P < 0.05; day 2, P < 0.01). The ratio of P70S6k(P) against total P70S6k on days 2 and 7 was significantly higher in SLOW than in the control. The ratio of FOXOl against total FOXOl, the ratio of FOXO3a against total FOXO3a, and myostatin on days 2 and 7 were significantly higher in FAST than in the control, while that of ActRIIB on day 7 was significantly lower in SLOW than in the other two groups. These results suggest that EC intensity plays a key role in impairment of muscular function and activation of protein synthesis and/or protein degradation signaling pathways.

Original languageEnglish
Pages (from-to)306-313
Number of pages8
JournalJournal of Applied Physiology
Volume108
Issue number2
DOIs
Publication statusPublished - Feb 1 2010

Keywords

  • Atrophy-related protein
  • Hypertrophy
  • Protein metabolism
  • Recovery
  • Speed

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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