AJP - Regu Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 297: R26-R33, 2009. First published April 1, 2009; doi:10.1152/ajpregu.90617.2008
0363-6119/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figures and Tables
Right arrow All Versions of this Article:
297/1/R26    most recent
90617.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Rehn, T. A.
Right arrow Articles by Iversen, P. O.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rehn, T. A.
Right arrow Articles by Iversen, P. O.

ARTICLES

Temporary fatigue and altered extracellular matrix in skeletal muscle during progression of heart failure in rats

Tommy A. Rehn,1,2,* Bengt Å. Borge,3,* Per K. Lunde,1,2 Morten Munkvik,1,2 Marianne Lunde Sneve,1,2 Frøy Grøndahl,5 Jan M. Aronsen,1,2 Ivar Sjaastad,1,2,4 Kristian Prydz,5 Svein O. Kolset,6 Helge Wiig,3 Ole M. Sejersted,1,2 and Per O. Iversen6,7

1Institute for Experimental Medical Research, Oslo University Hospital-Ullevaal, Oslo, Norway; 2Center for Heart Failure Research, University of Oslo, Oslo, Norway; 3Department of Biomedicine, University of Bergen, Bergen, Norway; 4Department of Cardiology, Oslo University Hospital-Ullevaal, Oslo, Norway; 5Department of Molecular Biosciences, University of Oslo, Oslo, Norway; 6Department of Nutrition, Faculty of Medicine, University of Oslo, Oslo, Norway; and 7Department of Hematology, Oslo University Hospital-Ullevaal, Oslo, Norway

Submitted 21 July 2008 ; accepted in final form 30 March 2009

Patients with congestive heart failure (CHF) experience increased skeletal muscle fatigue. The mechanism underlying this phenomenon is unknown, but a deranged extracellular matrix (ECM) might be a contributing factor. Hence, we examined ECM components and regulators in a rat postinfarction model of CHF. At various time points during a 3.5 mo-period after induction of CHF in rats by left coronary artery ligation, blood, interstitial fluid (IF), and muscles were sampled. Isoflurane anesthesia was employed during all surgical procedures. IF was extracted by wicks inserted intermuscularly in a hind limb. We measured cytokines in plasma and IF, whereas matrix metalloproteinase (MMP) activity and collagen content, as well as the level of glycosaminoglycans and hyaluronan were determined in hind limb muscle. In vivo fatigue protocols of the soleus muscle were performed at 42 and 112 days after induction of heart failure. We found that the MMP activity and collagen content in the skeletal muscles increased significantly at 42 days after induction of CHF, and these changes were time related to increased skeletal muscle fatigability. These parameters returned to sham levels at 112 days. VEGF in IF was significantly lower in CHF compared with sham-operated rats at 3 and 10 days, but no difference was observed at 112 days. We conclude that temporary alterations in the ECM, possibly triggered by VEGF, are related to a transient development of skeletal muscle fatigue in CHF.

fatigue; extracellular matrix; interstitial fluid; ischemic heart failure


Address for reprint requests and other correspondence: T. A. Rehn, Institute for Experimental Medical Research, Oslo Univ. Hospital-Ullevaal, N-0407 Oslo, Norway (e-mail: t.a.rehn{at}medisin.uio.no)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.