Potassium (K+) displacement in skeletal muscle may be an important factor in the development of muscle fatigue during intense exercise. It has been shown in vitro that an increase in the extracellular K+ concentration ([K+]e) to values higher than approx. 10 mm significantly reduce force development in unfatigued skeletal muscle. Several in vivo studies have shown that [K+]e increases progressively with increasing work intensity, reaching values higher than 10 mm. This increase in [K+]e is expected to be even higher in the transverse (T)‐tubules than the concentration reached in the interstitium. Besides the voltage‐sensitive K+ (Kv) channels that generate the action potential (AP) it is suggested that the big‐conductance Ca2+‐dependent K+ (KCa1.1) channel contributes significantly to the K+ release into the T‐tubules. Also the ATP‐dependent K+ (KATP) channel participates, but is suggested primarily to participate in K+ release to the interstitium. Because there is restricted diffusion of K+ to the interstitium, K+ released to the T‐tubules during AP propagation will be removed primarily by reuptake mediated by transport proteins located in the T‐tubule membrane. The most important protein that mediates K+ reuptake in the T‐tubules is the Na+,K+‐ATPase α2 dimers, but a significant contribution of the strong inward rectifier K+ (Kir2.1) channel is also suggested. The Na+, K+, 2Cl− 1 (NKCC1) cotransporter also participates in K+ reuptake but probably mainly from the interstitium. The relative content of the different K+‐transporting proteins differs in oxidative and glycolytic muscles, and might explain the different [K+]e tolerance observed.