Guest guest Posted August 23, 2007 Report Share Posted August 23, 2007 " Compared to normal littermates, the voluntary daily running distance was 1·8-fold greater in mice with a disruption of the gene for TNF & #945;, and 3-fold greater in mice with a gene disruption for both TNF & #945; and LT [lymphotoxin alpha]. " Looks like TNF may dampen motor drive even in healthy mammals. That is, if you believe that homozygous C57Bl/6 J mice are healthy mammals. This ain't no ecosystem. If the mice have any subtle parasites, those parasites have had many generations to adapt to the single identical C57Bl/6 J genotype. The way the mice are bred is equivalent to asexual reproduction. Not a lot of asexual vertebrate taxa out there, are there (there are a handful). I digress. Anyway, the normal C57Bl/6 J mice voluntarily run 3-4 km per day in an exercise wheel, which seems pretty frisky to me. The double knockout dudes covered 10 km a day! One of these guys is actually at the " Nijmegen Expertise Centre on Chronic Fatigue " in the Netherlands, and CFS is mentioned in the paper. They basically seem to favor a central (CNS) seat of fatigue in CFS, MS, and late cancer, not a peripheral abnormality. They don't review anything on objective abnormalities in CFS associated with energy metabolism and/or exercise. I think there are some. I haven't read em. Since I think(?) there's some evidence for cytokine transporters across the BBB, one should distinguish a purely-central fatigue physiology from a semi-central one in which peripheral cytokines pass into the CNS. Quote Link to comment Share on other sites More sharing options...
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