Document Detail

Exercise capacity in chronic heart failure patients is related to active gene transcription in skeletal muscle and not apoptosis.
MedLine Citation:
PMID:  19318954     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Muscle wasting partly explains exercise intolerance in chronic heart failure (CHF) patients. Skeletal muscle loss may result from apoptosis, and exercise training has been suggested to halt this process. The terminal deoxynucleotidyl transferase end-labeling (TUNEL) technique is frequently used to show apoptosis, but lacks specificity.
METHODS AND RESULTS: Before and after 4 months exercise training, skeletal muscle biopsies of 16 CHF patients (59.4+/-2.2 years, 11 men, 50% ischemic etiology, ejection fraction 28.8+/-2.7%, 66.3+/-3.6% of predicted oxygen uptake) and eight sedentary controls were analyzed for apoptosis (TUNEL, including the stringent variant without proteinase K digestion, immunohistochemical analyses using antibodies against cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase, PARP, and active gene transcription (anti-splicing factor SC-35). The number of TUNEL-positive nuclei in CHF patients was comparable with controls (3.2+/-0.7 vs. 3.1+/-1.7/mm(2), P=0.2) and was not related to exercise parameters. With the stringent TUNEL and both immunostaining techniques, apoptosis was not detected. Co-occurrence of TUNEL and of SC-35 splicing factor suggests that at least part of TUNEL-positive nuclei is undergoing active gene transcription and therefore is not apoptotic. The SC-35-positive area correlated with % of predicted oxygen uptake (r=0.6, P=0.02), Wattmax (r=0.7, P=0.005) and VE/VCO2 slope (r=-0.6, P=0.03). At baseline, SC-35 immunoreactive area was significantly larger than in controls (P=0.001), but after exercise training, the difference was minimized (P=0.07).
CONCLUSION: Skeletal muscle apoptosis in CHF patients could not be confirmed. Active gene transcription might stain false positive for apoptotic nuclei with TUNEL. The level of active gene transcription/splicing was related to exercise performance.
Viviane Marie Conraads; Vicky Y Hoymans; Tinie Vermeulen; Paul Beckers; Nadine Possemiers; Marianne De Maeseneer; Christiaan Vrints; Wim Martinet
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Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of cardiovascular prevention and rehabilitation : official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology     Volume:  16     ISSN:  1741-8275     ISO Abbreviation:  Eur J Cardiovasc Prev Rehabil     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-07-17     Completed Date:  2009-09-24     Revised Date:  2011-09-27    
Medline Journal Info:
Nlm Unique ID:  101192000     Medline TA:  Eur J Cardiovasc Prev Rehabil     Country:  England    
Other Details:
Languages:  eng     Pagination:  325-32     Citation Subset:  IM    
Department of Cardiology, University Hospital of Antwerp, Edegem, Belgium.
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MeSH Terms
Caspase 3 / metabolism
Chronic Disease
Exercise Therapy*
False Positive Reactions
Heart Failure / genetics,  pathology,  physiopathology,  therapy*
In Situ Nick-End Labeling
Middle Aged
Muscle, Skeletal / metabolism,  pathology,  physiopathology*
Muscular Atrophy / genetics,  pathology,  physiopathology,  prevention & control*
Nuclear Proteins / metabolism
Poly(ADP-ribose) Polymerases / metabolism
Reproducibility of Results
Resistance Training*
Ribonucleoproteins / metabolism
Time Factors
Transcription, Genetic*
Treatment Outcome
Reg. No./Substance:
0/Nuclear Proteins; 0/Ribonucleoproteins; 147153-65-9/SRSF2 protein, human; EC Polymerases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3

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