]. In this study, there was a strong inverse correlation of the total body potassium and the total time spent resting as a measure of fatigue and exhaustion. Lower plasma potassium levels were also found in a recent study in patients with ME/CFS compared with healthy controls [
]. If potassium leaving the cell during the process of repolarization via potassium channels is not taken up fast enough by the Na-ATPase in the working muscles, it reaches the blood stream to be renally excreted so that loss of potassium occurs during exercise. Thus, the indirect evidence for a lowered intracellular potassium together with our direct demonstration of a rise in intracellular sodium provides very strong arguments for a diminished Na+/K+-ATPase activity in ME/CFS.
Since it is technically not possible to measure intracellular sodium during exercise the possibility exists that sodium rises much higher than we measured pre- and post-exercise. During exercise sodium loading must be higher compared with rest because of sodium entry via sodium channels in the process of excitation which adds to sodium import via ion transporters of whom NHE1 may be the most important one.
The intensity values of the 4 reference phantoms with different NaCl solutions allowed us to measure sodium content via the signal intensities. After translating intensity to concentration in a linear trend analysis, we used mM as the unit to express tissue sodium content. However, it should be noted that with the methods of our scan protocol the signal decays very quickly and parts of tissue sodium are no longer visible and measurable at the time of measurement.
We measured total sodium content in muscle tissue and small vessels which supply muscle tissue. Long- and short-lived sodium components are measurable viaNa-MRI. The long-lived components are assumed to be the mobile, liquid sodium, which is mainly extracellular sodium and short-lived sodium is assumed to be intracellular sodium. Since only about 30% of the short-lived sodium is still visible at TE 2.
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