title: Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise.
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 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.
authors.affiliation: Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway. o.m.sejersted@ioks.uio.no
authors.forename: O M
authors.initials: OM
authors.lastname: Sejersted
authors.forename: G
authors.initials: G
authors.lastname: Sjøgaard
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000375:Aging / Q000378:metabolism; D000818:Animals; D001825:Body Fluid Compartments / Q000502:physiology; D005110:Extracellular Space / Q000378:metabolism; D005221:Fatigue / Q000378:metabolism; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D017136:Ion Transport / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009928:Organ Specificity / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D011188:Potassium / Q000378:metabolism* / Q000493:pharmacokinetics; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012508:Sarcolemma / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism
chemical_list: D015221:Potassium Channels; D020033:Protein Isoforms; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium