Article

Chronic fatigue syndrome combines increased exercise-induced oxidative stress and reduced cytokine and Hsp responses

Faculté de Médecine, Aix-Marseille Université, Marsiglia, Provence-Alpes-Côte d'Azur, France
Journal of Internal Medicine (Impact Factor: 6.06). 06/2009; 266(2):196-206. DOI: 10.1111/j.1365-2796.2009.02079.x
Source: PubMed

ABSTRACT

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.
This case-control study compared nine CFS patients to a gender-, age- and weight-matched control group of nine healthy sedentary subjects.
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.
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.
The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress, which might result from delayed and insufficient Hsp production.

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    • "TBARS increase 5 min after starting an incremental cycling exercise but increase also 2 days after exercise with maximal strength attributed to macrophage infiltrationand xanthine-oxidase activation-triggered reperfusion of the ischemic muscle[2]. Increase of TBARS during exercise is accompanied by reduced heat shock protein (HSP) production, suggesting that oxidative stress during exercise results from insufficient production of HSP[78]. Glutathione (GSH). "
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    • "The positive correlations between small Hsps and DJ-1 may be explained by increased ROS production. For example, in exercising muscles, increased levels of Hsp27 were associated with lower TBARS levels, suggesting that these Hsps may lower oxidative stress status [30]. In conclusion, increased ROS production may have induced simultaneously higher levels of DJ-1 and small Hsps. "
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