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Physiological Reviews, Vol. 80, No. 4, October 2000, pp. 1411-1481
Copyright ©2000 by the American Physiological Society
Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway; Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense; and National Institute of Occupational Health, Copenhagen, Denmark
Sejersted, Ole M. and
Gisela Sjøgaard.
Dynamics and Consequences of Potassium Shifts in Skeletal
Muscle and Heart During Exercise. Physiol. Rev. 80: 1411-1481, 2000.
Since it became
clear that K+ shifts with exercise are extensive and can
cause more than a doubling of the extracellular [K+]
([K+]s) as reviewed here, it has been
suggested that these shifts may cause fatigue through the effect on
muscle excitability and action potentials (AP). The cause of the
K+ shifts is a transient or long-lasting mismatch
between outward repolarizing K+ currents and K+
influx carried by the Na+-K+ pump. Several
factors modify the effect of raised [K+]s
during exercise on membrane potential (Em) and
force production. 1) Membrane conductance to K+
is variable and controlled by various K+ channels. Low
relative K+ conductance will reduce the contribution of
[K+]s to the Em. In
addition, high Cl
conductance may stabilize the
Em during brief periods of large K+
shifts. 2) The Na+-K+ pump
contributes with a hyperpolarizing current. 3) Cell swelling accompanies muscle contractions especially in fast-twitch muscle, although little in the heart. This will contribute considerably to the
lowering of intracellular [K+]
([K+]c) and will attenuate the
exercise-induced rise of intracellular [Na+]
([Na+]c). 4) The rise of
[Na+]c is sufficient to activate the
Na+-K+ pump to completely compensate increased
K+ release in the heart, yet not in skeletal muscle. In
skeletal muscle there is strong evidence for control of pump activity
not only through hormones, but through a hitherto unidentified
mechanism. 5) Ionic shifts within the skeletal muscle t
tubules and in the heart in extracellular clefts may markedly affect
excitation-contraction coupling. 6) Age and state of
training together with nutritional state modify muscle K+
content and the abundance of Na+-K+ pumps. We
conclude that despite modifying factors coming into play during muscle
activity, the K+ shifts with high-intensity exercise
may contribute substantially to fatigue in skeletal muscle, whereas in
the heart, except during ischemia, the K+ balance is
controlled much more effectively.
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