Potassium and fatigue: the pros and cons

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Abstract
A general finding is that muscle activity leads to potassium fluxes across the muscle membrane as well as to muscle fatigue, defined as a reduction in the force-generating capacity of the muscle. However, much controversy exists regarding the causal role of potassium in fatigue development. The experimental model used is decisive in this context, e.g. whether we study intact in vivo organs in situ with voluntary contractions and reflex feedback for cardiorespiratory regulation, or whether we study in vitro isolated muscles or cells-or even skinned fibres. In the latter models, clear evidence has been presented that Ca2+ is the variable significant for force development and that K+ may be ignored. However, in the in situ situation the limiting link in the chain leading to muscle contraction may be one preventing the Ca2+ release from taking place. The sites are the triads, T-tubules, and the surface membrane. The function of the latter two regarding action potential amplitude and propagation depends on [K+] gradients. Again, conflicting results exist regarding the electrophysiological changes and [K+] in fatigue. The activity pattern must then be taken into consideration. During high-intensity (high-frequency) activity the increased interstitial [K+] has been demonstrated to relate to fatigue, while in low-intensity fatiguing protocols, the T-tubule may be the limiting site. This fits with the concept of interstitial [K+] playing an essential role as a regulatory feedback mechanism, e.g. adjusting muscle blood flow to the metabolic load during muscle activity.

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