%0 Journal Article %1 Seje_2000_1411 %A Sejersted, O. M. %A Sj�gaard, G. %D 2000 %J Physiol. Rev. %K 11015618 ATPase, Acid-Base Aging, Animals, Body Channels, Compartments, Contraction, Equilibrium, Exertion, Extracellular Fatigue, Fluid Fluid, Gov't, Humans, Intracellular Ion Isoforms, Membrane Muscle Muscle, Myocardium, Non-U.S. Organ Potassium Potassium, Potentials, Protein Research Sarcolemma, Skeletal, Space, Specificity, Support, Transport, {N}a$^{+}$-{K}$^{+}$-Exchanging %N 4 %P 1411--1481 %T Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise. %U http://physrev.physiology.org/cgi/content/full/80/4/1411 %V 80 %X 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 (E(m)) 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 E(m). In addition, high Cl$^-$ conductance may stabilize the E(m) 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.

@article{Seje_2000_1411, abstract = {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 {N}a$^{+}$-{K}$^{+}$ pump. Several factors modify the effect of raised [{K}$^{+}$](s) during exercise on membrane potential (E(m)) 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 E(m). In addition, high {C}l$^{-}$ conductance may stabilize the E(m) during brief periods of large {K}$^{+}$ shifts. 2) The {N}a$^{+}$-{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 [{N}a$^{+}$] ([{N}a$^{+}$](c)). 4) The rise of [{N}a$^{+}$](c) is sufficient to activate the {N}a$^{+}$-{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 {N}a$^{+}$-{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.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Sejersted, O. M. and Sj�gaard, G.}, biburl = {https://www.bibsonomy.org/bibtex/24e7f99c90cbb129070587b866bac0802/hake}, description = {The whole bibliography file I use.}, file = {Seje_2000_1411.pdf:Seje_2000_1411.pdf:PDF}, interhash = {bfc5e12adfdb275dc3d9438a2e8bb486}, intrahash = {4e7f99c90cbb129070587b866bac0802}, journal = {Physiol. Rev.}, key = 17, keywords = {11015618 ATPase, Acid-Base Aging, Animals, Body Channels, Compartments, Contraction, Equilibrium, Exertion, Extracellular Fatigue, Fluid Fluid, Gov't, Humans, Intracellular Ion Isoforms, Membrane Muscle Muscle, Myocardium, Non-U.S. Organ Potassium Potassium, Potentials, Protein Research Sarcolemma, Skeletal, Space, Specificity, Support, Transport, {N}a$^{+}$-{K}$^{+}$-Exchanging}, month = Oct, number = 4, pages = {1411--1481}, pmid = {11015618}, timestamp = {2009-06-03T11:21:29.000+0200}, title = {Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise.}, url = {http://physrev.physiology.org/cgi/content/full/80/4/1411}, volume = 80, year = 2000 }