Linked Life Data

9356761

Source:http://linkedlifedata.com/resource/pubmed/id/9356761

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1997-12-9
pubmed:abstractText
Definitive characterization of the mechanisms of skeletal muscle fatigue is still an area of active investigation. One emerging theory concerns a role for the reactive oxygen species (ROS) produced primarily as a consequence of elevated rates of mitochondrial respiration. It has been theorized that the long-lasting effects of low-frequency fatigue (LFF) can be attributed to disruption of some stage of the excitation contraction coupling (ECC) process. Recent evidence suggests that ROS likely denature one or more proteins directly associated with the sarcoplasmic reticulum (SR) Ca2+ release mechanism. Given the potential of ROS to damage intracellular proteins during subsequent bouts of muscle contractions, the capacity of preexisting antioxidant pathways may be complemented by the synthesis of inducible heat-stress proteins (HSPs). HSPs collectively function to maintain cellular protein conformation during stressful proteotoxic insults. The goal of this article is to illustrate how recent findings suggest a dual role of ROS generated during muscle contractions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1066-7814
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
409-28
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Muscle fatigue and induction of stress protein genes: a dual function of reactive oxygen species?
pubmed:affiliation
Department of Exercise Science, Blatt Center, University of South Carolina, Columbia 29208, USA.
pubmed:publicationType
Journal Article, Review