TY - JOUR
T1 - Potassium-transporting proteins in skeletal muscle: cellular location and fiber-type differences
AU - Kristensen, Michael
AU - Juel, Carsten
N1 - KEYWORDS
channels • cotransporters • distribution • exercise • Na+,K+-ATPase
PY - 2010
Y1 - 2010
N2 - 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 a2 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.
AB - 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 a2 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.
U2 - 10.1111/j.1748-1716.2009.02043.x
DO - 10.1111/j.1748-1716.2009.02043.x
M3 - Journal article
C2 - 19769637
SN - 1748-1708
VL - 198
SP - 105
EP - 123
JO - Acta Physiologica (Print Edition)
JF - Acta Physiologica (Print Edition)
IS - 2
ER -