Linked Life Data

19959771

Source:http://linkedlifedata.com/resource/pubmed/id/19959771

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-2-1
pubmed:abstractText
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 degrees/s; n = 12), slow ECs group (SLOW; 30 degrees/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 (FOXO1), FOXO1(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 FOXO1 against total FOXO1, 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1522-1601
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
306-13
pubmed:dateRevised
2010-10-8
pubmed:meshHeading
pubmed-meshheading:19959771-Activin Receptors, Type II, pubmed-meshheading:19959771-Animals, pubmed-meshheading:19959771-Atrophy, pubmed-meshheading:19959771-Biomechanics, pubmed-meshheading:19959771-Blotting, Western, pubmed-meshheading:19959771-Body Weight, pubmed-meshheading:19959771-Forkhead Transcription Factors, pubmed-meshheading:19959771-Hypertrophy, pubmed-meshheading:19959771-Isometric Contraction, pubmed-meshheading:19959771-Joints, pubmed-meshheading:19959771-Male, pubmed-meshheading:19959771-Muscle, Skeletal, pubmed-meshheading:19959771-Muscle Contraction, pubmed-meshheading:19959771-Muscle Proteins, pubmed-meshheading:19959771-Myostatin, pubmed-meshheading:19959771-Nerve Tissue Proteins, pubmed-meshheading:19959771-Organ Size, pubmed-meshheading:19959771-Rats, pubmed-meshheading:19959771-Rats, Wistar, pubmed-meshheading:19959771-Signal Transduction, pubmed-meshheading:19959771-Transforming Growth Factor beta
pubmed:year
2010
pubmed:articleTitle
Elevation of myostatin and FOXOs in prolonged muscular impairment induced by eccentric contractions in rat medial gastrocnemius muscle.
pubmed:affiliation
Laboratory of Health and Sports Sciences, Center for Liberal Arts, Meiji Gakuin Univ., 1518 Kamikurata-cho, Totsuka-ku, Yokohama, Kanagawa 244-8539, Japan. ochi@gen.meijigakuin.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't