title: Chronic fatigue syndrome combines increased exercise-induced oxidative stress and reduced cytokine and Hsp responses.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  This case-control study compared nine CFS patients to a gender-, age- and weight-matched control group of nine healthy sedentary subjects.
  
  
  METHODS
  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.
authors.affiliation: UMR MD2 (P2COE), Faculté de Médecine, Université de la Méditerranée, North Hospital, Assistance Publique - Hôpitaux de Marseille, France. yves.jammes@univmed.fr
authors.forename: Y
authors.initials: Y
authors.lastname: Jammes
authors.forename: J G
authors.initials: JG
authors.lastname: Steinberg
authors.forename: S
authors.initials: S
authors.lastname: Delliaux
authors.forename: F
authors.initials: F
authors.lastname: Brégeon
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism*; D004576:Electromyography; D015444:Exercise / Q000502:physiology*; D015673:Fatigue Syndrome, Chronic / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D055551:HSP27 Heat-Shock Proteins / Q000097:blood; D018840:HSP70 Heat-Shock Proteins / Q000097:blood; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D016014:Linear Models; D008297:Male; D018384:Oxidative Stress; D011659:Pulmonary Gas Exchange; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D016207:Cytokines; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D015850:Interleukin-6; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D001205:Ascorbic Acid