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1 Abteilung für Sport-
und Arbeitsphysiologie,
K+ released from exercising
muscle via K+ channels needs to be
removed from the interstitium into the blood to maintain high muscle
cell membrane potential and allow normal muscle contractility. Uptake
by red blood cells has been discussed as one mechanism that would also
serve to regulate red blood cell volume, which was found to be constant
despite increased plasma osmolality and K+ concentration
([K+pl]). We evaluated
exercise-related changes in
[K+pl], pH, osmolality, mean
cellular Hb concentration, cell water, and red blood cell
K+ concentration during exhaustive
handgrip exercise. Unidirectional 86Rb+
(K+) uptake by red blood cells
was measured in media with elevated extracellular
K+, osmolarity, and
catecholamines to simulate particularly those exercise-related changes
in plasma composition that are known to stimulate
K+ uptake. During exercise
[K+pl] increased from 4.4 ± 0.7 to 7.1 ± 0.5 mmol/l plasma water and red blood cell K+ concentration increased from
137.2 ± 6.0 to 144.6 ± 4.6 mmol/l cell water
(P 
0.05), but the intracellular
K+-to-mean cellular
Hb concentration ratio did not change.
86Rb+
uptake by red blood cells was increased by ~20% on stimulation, caused by activation of the
Na+-K+
pump and
Na+-K+-2Cl
cotransport. Results indicate the
K+ content of red blood cells did
not change as cells passed the exhaustively exercising forearm muscle
despite the elevated [K+pl]. The tendency for an increase in intracellular
K+ concentration was due to a
slight, although statistically not significant, decrease in red blood
cell volume. K+ uptake, although
elevated, was too small to move significant amounts of
K+ into red blood cells. Our
results suggest that red blood cells do not contribute to the removal
of K+ released from muscle and do
not regulate their volume by K+
uptake during exhaustive forearm exercise.
potassium; muscle; red blood cell volume; potassium uptake; sodium-potassium pump; sodium-potassium-2-chloride cotransport
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