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Sökning: onr:"swepub:oai:DiVA.org:oru-64016" > Exercise induces is...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005451naa a2200505 4500
001oai:DiVA.org:oru-64016
003SwePub
008180110s2000 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:1961736
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-640162 URI
0247 a https://doi.org/10.1006/bbrc.2000.30732 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:19617362 URI
040 a (SwePub)orud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Fujii, N.u Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA4 aut
2451 0a Exercise induces isoform-specific increase in 5'AMP-activated protein kinase activity in human skeletal muscle
264 1a San Diego, CA, USA :b Academic Press,c 2000
338 a print2 rdacarrier
500 a Funding Agency:NIAMS NIH HHS
520 a The 5'AMP-activated protein kinase (AMPK) is stimulated by contractile activity in rat skeletal muscle. AMPK has emerged as an important signaling intermediary in the regulation of cell metabolism being linked to exercise-induced changes in muscle glucose and fatty acid metabolism. In the present study, we determined the effects of exercise on isoform-specific AMPK activity (alpha1 and alpha2) in human skeletal muscle. Needle biopsies of vastus lateralis muscle were obtained from seven healthy subjects at rest, after 20 and 60 min of cycle ergometer exercise at 70% of VO(2)max, and 30 min following the 60 min exercise bout. In comparison to the resting state, AMPK alpha2 activity significantly increased at 20 and 60 min of exercise, and remained at a higher level with 30 min of recovery. AMPK alpha1 activity tended to slightly decrease with 20 min of exercise at 70%VO(2)max; however, the change was not statistically significant. AMPK alpha1 activities were at basal levels at 60 min of exercise and 30 min of recovery. On a separate day, the same subjects exercised for 20 min at 50% of VO(2)max. Exercise at this intensity did not change alpha2 activity, and similar to exercise at 70% of VO(2)max, there was no significant change in alpha1 activity. In conclusion, exercise at a higher intensity for only 20 min leads to increases in AMPK alpha2 activity but not alpha1 activity. These results suggest that the alpha2-containing AMPK complex, rather than alpha1, may be involved in the metabolic responses to exercise in human skeletal muscle.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Fysiologi0 (SwePub)301062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Physiology0 (SwePub)301062 hsv//eng
653 a AMPK
653 a exercise
653 a glucose transport
653 a skeletal
7001 a Hayashi, T.u Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA4 aut
7001 a Hirshman, M.u Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA4 aut
7001 a Smith, J.u Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA4 aut
7001 a Habonowski, S.u Endocrine-Metabolism Division, Department of Medicine and Biochemistry, Dartmouth Medical School, Hanover, New Hampshire, USA4 aut
7001 a Kaijser, L.u Karolinska Institutet4 aut
7001 a Mu, J.u Howard Hughes Medical Institute, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA4 aut
7001 a Ljungqvist, Olle,d 1954-u Karolinska Institutet,Örebro universitet,Institutionen för medicinska vetenskaper,Region Örebro län,Department of Surgery, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden; Center of Gastrointestinal Disease, Ersta Hospital, Karolinska Institute, Stockholm, Sweden4 aut0 (Swepub:oru)olt
7001 a Birnbaum, M.u Howard Hughes Medical Institute, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA4 aut
7001 a Witters, L.u Endocrine-Metabolism Division, Department of Medicine and Biochemistry, Dartmouth Medical School, Hanover, New Hampshire, USA4 aut
7001 a Thorell, A.u Karolinska Institutet4 aut
7001 a Goodyear, L.u Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA4 aut
7102 a Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USAb Endocrine-Metabolism Division, Department of Medicine and Biochemistry, Dartmouth Medical School, Hanover, New Hampshire, USA4 org
7730 t Biochemical and Biophysical Research Communications - BBRCd San Diego, CA, USA : Academic Pressg 273:3, s. 1150-1155q 273:3<1150-1155x 0006-291Xx 1090-2104
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-64016
8564 8u https://doi.org/10.1006/bbrc.2000.3073
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:1961736

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