Linked Life Data

1464836

Source:http://linkedlifedata.com/resource/pubmed/id/1464836

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-1-15
pubmed:abstractText
1. The role of the myoplasmic free Mg2+ concentration ([Mg2+]i) in fatigue was studied in intact single fibres isolated from mouse skeletal muscle. Fatigue was produced by repeated tetanic stimulation. The fluorescent Mg2+ indicator furaptra was pressure injected into fibres. In vivo calibrations were performed to convert fluorescence signals into [Mg2+]i. 2. [Mg2+]i at rest was 0.78 +/- 0.05 mM (mean +/- S.E.M., n = 14). An increase of the extracellular [Mg2+] from 0.5 to 20 mM resulted in a small elevation of [Mg2+]i (86 microM in 5 min). Removal of extracellular Na+ did not affect [Mg2+]i. An intracellular alkanization of about 0.6 pH units gave a [Mg2+]i reduction of 65 microM. 3. During fatiguing stimulation [Mg2+]i initially remained almost constant and it then suddenly started to rise towards the end of the stimulation period. The onset of the [Mg2+]i rise was always followed by a rapid tension decline. In fatigue [Mg2+]i was approximately twice as high as at rest. 4. Fibres were injected with MgCl2 to study if the rise in [Mg2+]i could explain the tension decline in fatigue. An elevation of [Mg2+]i was accompanied by a tension reduction but the [Mg2+]i for a given tension was generally much higher in rested fibres injected with MgCl2 than in fatigued fibres. Thus the rise in [Mg2+]i as such cannot explain the tension reduction in fatigue. 5. Injection of MgCl2 was also used to assess the intracellular Mg2+ buffering. The mean Mg2+ buffer power (i.e. the ratio of the change in [Mg2+]i to the amount of Mg2+ added) was 0.62. 6. ATP is the quantitatively most important binding site for Mg2+ at rest and ATP breakdown is then a likely source of the [Mg2+]i increase in fatigue. The role of ATP breakdown in the increase of [Mg2+]i was studied with metabolic inhibition: fibres were exposed to iodoacetic acid to inhibit glycolysis and cyanide to inhibit oxidative phosphorylation. The pattern during metabolic inhibition was similar to that observed during fatigue. After remaining almost constant during a lengthy period, [Mg2+]i rose rapidly and this rise preceded a period of rapid tension decline. The fibres thereafter went into rigor and [Mg2+]i stabilized at an elevated level; the mean [Mg2+]i increase in rigor was 1.30 mM. 7. We have used modelling to determine the likely change in the intracellular ATP concentration ([ATP]i) for the observed changes in [Mg2+]i.(ABSTRACT TRUNCATED AT 400 WORDS)
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-13807760, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1522520, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1708823, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1761971, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1830458, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1841942, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1902515, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-1902516, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2011468, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2016581, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2191782, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2352837, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2354505, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2381762, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2410798, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2442362, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2729592, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-28541, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-2923192, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3231093, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3266079, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3286252, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3443937, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3552284, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3621285, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3754147, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-4650939, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-5647260, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-566428, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-6309755, http://linkedlifedata.com/resource/pubmed/commentcorrection/1464836-7195747
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:volume
453
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-34
pubmed:dateRevised
2010-9-7
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Myoplasmic free Mg2+ concentration during repetitive stimulation of single fibres from mouse skeletal muscle.
pubmed:affiliation
Department of Physiology, University of Sydney, NSW, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't