Myostatin dysfunction impairs force generation in extensor digitorum longus muscle and increases exercise-induced protein efflux from extensor digitorum longus and soleus muscles

Juozas Baltusnikas, Audrius Kilikevicius, Tomas Venckunas, Andrej Fokin, Lutz Bunger, Arimantas Lionikas, Aivaras Ratkevicius

Research output: Contribution to journalArticle

2 Citations (Scopus)
6 Downloads (Pure)

Abstract

Myostatin dysfunction promotes muscle hypertrophy which can complicate assessment of muscle properties. We examined force generating capacity and creatine kinase (CK) efflux from skeletal muscles of young mice before they reach adult body and muscle size. Isolated soleus (SOL) and extensor digitorum longus (EDL) muscles of Berlin high (BEH) mice with dysfunctional myostatin, i.e. homozygous for inactivating myostatin mutation, and with a wild type myostatin (BEH+/+) were studied. The muscles of BEH mice showed faster (P < 0.01) twitch and tetanus contraction times compared to BEH+/+ mice, but only EDL displayed lower (P < 0.05) specific force. SOL and EDL of age matched, but not younger BEH mice showed greater exercise-induced CK efflux compared to BEH+/+ mice. In summary, myostatin dysfunction leads to impairment in muscle force generating capacity in EDL and increases susceptibility of SOL and EDL to protein loss after exercise.
Original languageEnglish
Pages (from-to)817-821
Number of pages5
JournalApplied Physiology Nutrition and Metabolism / Physiologie Appliquée, Nutrition et Métabolisme
Volume40
Issue number8
Early online date6 Apr 2015
DOIs
Publication statusPublished - Aug 2015

Keywords

  • lengthening contractions
  • muscle force
  • muscle damage
  • myostatin

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