Hvorfor trening er så farlig for pasienter med ME/CFS

Posted on 02/07/2011


Hentet fra Facebooksiden til XMRV Global Advocacy. (Jeg har ikke referanser på de påstandene som blir gjort her, men det virker som en god oppsummering på fenomenet med aktivitetsutløst sykdomsforverring i tråd med den forskningen jeg har lest.)


People with ME have high levels of proinflammatory cytokines and oxidative stress.  Both are toxic and cause a range of neurological and bodily symptoms.

This also damages mitochondria.

Without working mitochondria our bodies won’t function and our minds won’t work.

Excercise increases oxidative stress and proinflammatory cytokines further damaging our mitochondria,  which makes us more ill and it takes a long time for our mitochondrial batteries to recharge.

Some recover, but some don’t and are left permanently disabled.  This is why GET is so dangerous and why anyone advocating increasing activity levels should be ignored.

Even doing more reading than normal could do a lot of damage.



Special Feature for the Olympics: Effects of Excercise on the Immune System

Immunology and Cell Biology (2000) 78, 532–535; doi:10.1111/j.1440-1711.2000.t01-11-.x

Exercise and cytokines

Bente Klarlund Pedersen1

1The Copenhagen Muscle Research Centre, Department of Infectious Diseases, University of Copenhagen, Copenhagen, Denmark

Correspondence: Bente Klarlund Pedersen, Department of Infectious Diseases M7721, Rigshospitalet, Tagensvej 20, 2200 Copenhagen N, Denmark. Email: bkp@rh.dk

Received 26 June 2000; Accepted 26 June 2000.


Strenuous exercise induces increased levels in a number of pro-inflammatory and anti-inflammatory cytokines, naturally occurring cytokine inhibitors and chemokines. Thus, increased plasma levels of TNF-, IL-1, IL-6, IL-1receptor antagonist, TNF receptors, IL-10, IL-8 and macrophage inflammatory protein-1 are found after strenuous exercise. The concentration of IL-6 increases up to 100-fold after a marathon race. The increase in IL-6 is tightly related to the duration of the exercise and there appears to be a logarithmic relationship. Furthermore, the increase in IL-6 is related to the intensity of exercise. Given the facts that IL-6, more than any other cytokine, is produced in large amounts in response to exercise, that IL-6 is produced locally in the skeletal muscle in response to exercise and that IL-6 is known to have growth factor abilities, it is likely that IL-6 plays a beneficial role and may be involved in mediating exercise-related metabolic changes.


Posted in: Forskning