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Chronic fatigue
syndrome intracellular immune deregulations
as a possible
etiology for abnormal exercise response
Jo
Nijs, Kenny De Meirleir, Mira Meeus,
Neil R. McGregor and Patrick Englebienne
Received 1 October 2003;
Accepted
9 November 2003;
Available online 20 February 2004.
Abstract
The
exacerbation of symptoms after exercise differentiates Chronic fatigue
syndrome (CFS) from several other fatigue-associated disorders. Research
data point to an abnormal response to exercise in patients with CFS
compared to healthy sedentary controls, and to an increasing amount of
evidence pointing to severe intracellular immune deregulations in CFS
patients. This manuscript explores the hypothetical interactions between
these two separately reported observations. First, it is explained that
the deregula-tion of the 2-5A synthetase/RNase L
pathway may be related to a channelopathy, capable of initiating both
intracellular hypomagnesaemia in skeletal muscles and transient
hypoglycemia. This might explain muscle weakness and the reduction of
maximal oxygen uptake, as typically seen in CFS patients. Second, the
activation of the protein kinase R (PKR) enzyme,
a characteristic feature in at least subsets of
CFS patients, might account for the observed excessive nitric oxide (NO)
production in patients with CFS. Elevated NO is known to induce vasodilation,
which may limit CFS patients to increase blood flow during exercise, and
may even cause and enhanced post-exercise
hypotension. Finally, it is explored how several types of infections,
frequently identified in CFS patients, fit into these hypothetical
pathophysiological interactions.
Opmerking: PKR en RNAse-L
worden geproduceerd na blootstelling aan chemicalien of infekties, FT!! |
