The DOI matches its Crossref record; 448 of the 448 references it cites were found in a registry or an index.
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.
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Metadata
- Authors
- Sejersted, O. M., & Sjøgaard, G.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2000-01-10
- Volume
- 80
- Issue
- 4
- Pages
- 1411-1481
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2156262323
- Cited by
- 490
- References
- 448
- FWCI
- 0.99
- Type
- journal article
- Language
- en
- Open access
- closed
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