Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise

Physiol Rev. 2000 Oct;80(4):1411-81. doi: 10.1152/physrev.2000.80.4.1411.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acid-Base Equilibrium / physiology
  • Aging / metabolism
  • Animals
  • Body Fluid Compartments / physiology
  • Extracellular Space / metabolism
  • Fatigue / metabolism
  • Humans
  • Intracellular Fluid / metabolism
  • Ion Transport / physiology
  • Membrane Potentials / physiology
  • Muscle Contraction / physiology
  • Muscle, Skeletal / metabolism*
  • Myocardium / metabolism*
  • Organ Specificity / physiology
  • Physical Exertion / physiology*
  • Potassium / metabolism*
  • Potassium / pharmacokinetics
  • Potassium Channels / genetics
  • Potassium Channels / metabolism
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Sarcolemma / metabolism
  • Sodium-Potassium-Exchanging ATPase / genetics
  • Sodium-Potassium-Exchanging ATPase / metabolism


  • Potassium Channels
  • Protein Isoforms
  • Sodium-Potassium-Exchanging ATPase
  • Potassium