The power and pitfalls of omics part 2: epigenomics, transcriptomics and ME/CFS
Simon McGrath concludes his blog about the remarkable Prof George Davey Smith's smart ideas for understanding diseases, which may soon be applied to ME/CFS.
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Exercise, immunity and redox status

Discussion in 'Other Health News and Research' started by kaffiend, Oct 21, 2011.

  1. kaffiend

    kaffiend Senior Member

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    I just came across this study in PLoS ONE. I haven't read it carefully, but at first glance it seems to fit nicely with Rich Van Konynenburg's ideas on depleted glutathione and altered redox status.

    Severe Exercise and Exercise Training Exert Opposite Effects on Human Neutrophil Apoptosis via Altering the Redox Status

    Abstract
    Neutrophil spontaneous apoptosis, a process crucial for immune regulation, is mainly controlled by alterations in reactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity; while acute severe exercise (ASE) usually impedes immunity, chronic moderate exercise (CME) improves it. This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercise group (n = 8) underwent 2 months of CME followed by 2 months of detraining. Additional ASE paradigms were performed at the end of each month. Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying neutrophil spontaneous apoptosis (annexin-V binding on the outer surface) along with redox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathione level, retarded spontaneous apoptosis and delayed mitochondria deterioration; iii) most effects of CME were unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore, the ASE effects on neutrophil spontaneous apoptosis were mimicked by adding exogenous H2O2, but not by suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted in acceleration of human neutrophil apoptosis, CME delayed neutrophil apoptosis by maintaining a reduced state for long periods of time even after detraining.
     
  2. Valentijn

    Valentijn Senior Member

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    I'm no biochemist, but the general gist seems to be that moderate exercise is beneficial.

    The problem with this in ME/CFS there is probably usually a cysteine deficiency. Cysteine is needed to form Aconitase, an enzyme needed to convert most food into cellular energy. The symptoms of Aconitase deficiency include post-exertional malaise, muscle pain, and sometimes death when exercising.

    Moderate exercise is probably very beneficial in the way listed in this study, but the adverse side effects vastly outweigh the benefits for people with ME/CFS.
     
  3. kaffiend

    kaffiend Senior Member

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    I post this as a possible mechanism underlying post-exertional neuro-immune symptoms, not as a suggestion to take up moderate exercise. If the redox status is already poor in ME/CFS, then ANY physical activity will be seen as acute severe exercise. This fits with my own experience where walking to the car would be more exhausting than 100 mile cycling events.
     
  4. mellster

    mellster Marco

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    I do think there is benefit also for ME/CFS patients in mild/moderate exercise - the definition of moderate exercise obviously varies greatly depending on level of activity. Also I view this condition more like a sliding scale that possibly every human being can be affected with depending on whether and how often they cross their current individual exertion thresholds. It is not a surprise that quite a few athletes come down with it despite being in healthy and in excellent shape, it all depends on the amount of strain you put on your body and the momentary circumstances. Taking adequate supplements before and after exercise as well as anti-inflammatories (for possible cytokine response) might alleviate the post-exertional reactions. Thx for posting this.
     

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