Linked Life Data

21059760

Source:http://linkedlifedata.com/resource/pubmed/id/21059760

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 1
pubmed:dateCreated
2011-1-12
pubmed:abstractText
Creatine kinase (CK) plays a key role both in energy provision and in signal transduction for the increase in skeletal muscle O2 uptake () at exercise onset. The effects of acute CK inhibition by iodoacetamide (IA; 5 mm) on kinetics were studied in isolated canine gastrocnemius muscles in situ (n = 6) during transitions from rest to 3 min of electrically stimulated contractions eliciting ?70% of muscle peak , and were compared to control (Ctrl) conditions. In both IA and Ctrl muscles were pump-perfused with constantly elevated blood flows. Arterial and venous [O2] were determined at rest and every 5-7 s during contractions. was calculated by Fick's principle. Muscle biopsies were obtained at rest and after ?3 min of contractions. Muscle force was measured continuously. There was no fatigue in Ctrl (final force/initial force (fatigue index, FI) = 0.97 ± 0.06 (x ± s.d.)), whereas in IA force was significantly lower during the first contractions, slightly recovered at 15-20 s and then decreased (FI 0.67 ± 0.17). [Phosphocreatine] was not different in the two conditions at rest, and decreased during contractions in Ctrl, but not in IA. at 3 min was lower in IA (4.7 ± 2.9 ml 100 g-1 min-1) vs. Ctrl (16.6 ± 2.5 ml 100 g-1 min-1). The time constant (?) of kinetics was faster in IA (8.1 ± 4.8 s) vs. Ctrl (16.6 ± 2.6 s). A second control condition (Ctrl-Mod) was produced by modelling a response that accounted for the 'non-square' force profile in IA, which by itself could have influenced kinetics. However, ? in IA was faster than in Ctrl-Mod (13.8 ± 2.8 s). The faster kinetics due to IA suggest that in mammalian skeletal muscle in situ, following contractions onset, temporal energy buffering by CK slows the kinetics of signal transduction for the activation of oxidative phosphorylation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1469-7793
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
589
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
221-33
pubmed:meshHeading
pubmed-meshheading:21059760-Animals, pubmed-meshheading:21059760-Biopsy, pubmed-meshheading:21059760-Creatine Kinase, MM Form, pubmed-meshheading:21059760-Dogs, pubmed-meshheading:21059760-Electric Stimulation, pubmed-meshheading:21059760-Enzyme Inhibitors, pubmed-meshheading:21059760-Female, pubmed-meshheading:21059760-Iodoacetamide, pubmed-meshheading:21059760-Kinetics, pubmed-meshheading:21059760-Male, pubmed-meshheading:21059760-Models, Biological, pubmed-meshheading:21059760-Muscle, Skeletal, pubmed-meshheading:21059760-Muscle Contraction, pubmed-meshheading:21059760-Muscle Strength, pubmed-meshheading:21059760-Oxidative Phosphorylation, pubmed-meshheading:21059760-Oxygen, pubmed-meshheading:21059760-Oxygen Consumption, pubmed-meshheading:21059760-Perfusion, pubmed-meshheading:21059760-Phosphocreatine, pubmed-meshheading:21059760-Regional Blood Flow, pubmed-meshheading:21059760-Up-Regulation
pubmed:year
2011
pubmed:articleTitle
Faster O? uptake kinetics in canine skeletal muscle in situ after acute creatine kinase inhibition.
pubmed:affiliation
Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Udine, Piazzale M. Kolbe 4, I-33100 Udine, Italy. bruno.grassi@uniud.it
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural