Document Detail

Chronic fatigue syndrome combines increased exercise-induced oxidative stress and reduced cytokine and Hsp responses.
MedLine Citation:
PMID:  19457057     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: As heat shock proteins (Hsp) protect the cells against the deleterious effects of oxidative stress, we hypothesized that Hsp expression might be reduced in patients suffering from chronic fatigue syndrome (CFS) who present an accentuated exercise-induced oxidative stress. DESIGN: This case-control study compared nine CFS patients to a gender-, age- and weight-matched control group of nine healthy sedentary subjects. INTERVENTIONS: All subjects performed an incremental cycling exercise continued until exhaustion. We measured ventilation and respiratory gas exchange and evoked compound muscle potential (M-wave) recorded from vastus lateralis. Repetitive venous blood sampling allowed measurements of two markers of oxidative stress [thiobarbituric acid reactive substances (TBARS) and reduced ascorbic acid (RAA)], two cytokines (IL-6 and TNF-alpha) and two Hsp (Hsp27 and Hsp70) at rest, during maximal exercise and the 60-min recovery period. RESULTS: Compared with controls, resting CFS patients had low baseline levels of RAA and Hsp70. Their response to maximal exercise associated (i) M-wave alterations indicating reduced muscle membrane excitability, (ii) early and accentuated TBARS increase accompanying reduced changes in RAA level, (iii) absence of significant increase in IL-6 and TNF-alpha, and (iv) delayed and marked reduction of Hsp27 and Hsp70 variations. The post-exercise increase in TBARS was accentuated in individuals having the lowest variations of Hsp27 and Hsp70. CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress, which might result from delayed and insufficient Hsp production.
Y Jammes; J G Steinberg; S Delliaux; F Brégeon
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Publication Detail:
Type:  Journal Article     Date:  2009-05-19
Journal Detail:
Title:  Journal of internal medicine     Volume:  266     ISSN:  1365-2796     ISO Abbreviation:  J. Intern. Med.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-20     Completed Date:  2009-08-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8904841     Medline TA:  J Intern Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  196-206     Citation Subset:  IM    
UMR MD2 (P2COE), Faculté de Médecine, Université de la Méditerranée, North Hospital, Assistance Publique - Hôpitaux de Marseille, France.
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MeSH Terms
Analysis of Variance
Ascorbic Acid / blood
Biological Markers / blood
Case-Control Studies
Cytokines / metabolism*
Exercise / physiology*
Fatigue Syndrome, Chronic / metabolism*,  physiopathology
HSP27 Heat-Shock Proteins / blood
HSP70 Heat-Shock Proteins / blood
Heat-Shock Proteins / metabolism*
Interleukin-6 / blood
Linear Models
Oxidative Stress
Pulmonary Gas Exchange
Thiobarbituric Acid Reactive Substances / analysis
Tumor Necrosis Factor-alpha / blood
Reg. No./Substance:
0/Biological Markers; 0/Cytokines; 0/HSP27 Heat-Shock Proteins; 0/HSP70 Heat-Shock Proteins; 0/Heat-Shock Proteins; 0/Interleukin-6; 0/Thiobarbituric Acid Reactive Substances; 0/Tumor Necrosis Factor-alpha; 50-81-7/Ascorbic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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