Lindinger M I, McKelvie R S, Heigenhauser G J
School of Human Biology, University of Guelph, Canada.
J Appl Physiol (1985). 1995 Mar;78(3):765-77. doi: 10.1152/jappl.1995.78.3.765.
This review describes processes for the distribution of K+ ([K+]) and lactate concentrations ([Lac-]) that are released from contracting muscle at high rates during high-intensity exercise. This results in increased interstitial and venous [K+] and [Lac-] in contracting muscle. Large and rapid increases in plasma [K+] and [Lac-] result in the transport of these ions into red blood cells (RBCs). These ions are distributed to noncontracting tissues within both the plasma and RBC compartments of blood. The extraction of K+ and Lac- from the circulation by noncontracting tissue serves to markedly attenuate exercise-induced increases in plasma [K+] and [Lac-]. This apparent regulation of the plasma compartment by noncontracting tissues helps to maintain favorable concentration gradients for the net movement of [K+] and [Lac-] into the venous side of the microcirculation from interstitial fluids of contracting muscle. This provides conditions that 1) reduce the increase in interstitial [K+], thereby decreasing the magnitude and rate of sarcolemmal depolarization, and 2) favor the sarcolemmal transport of Lac- from within contracting muscle cells, thereby regulating intracellular osmolality and H+ concentration. On cessation of exercise, net K+ uptake by recovering muscle is rapid, with 90-95% recovery of intracellular [K+] within 3.5 min, indicating a very high rate of Na+-K+ pump activity. The K+ extracted by noncontracting tissues during exercise may be slowly released during recovery. During the initial minutes of recovery, recovering muscle continues to release Lac- into the circulation, and noncontracting tissues continue to extract Lac- for up to 30 min. The uptake of Lac- by noncontracting tissues results in elevated intracellular [Lac-]. There is no evidence that Lac- extracted by noncontracting tissues is subsequently released; it is probably metabolized within these cells. We conclude that the uptake of K+ and Lac- by RBCs and noncontracting tissues regulates ion homeostasis within plasma and the interstitial and intracellular compartments of contracting muscle. The regulatory processes help to maintain the function of active muscles by delaying the onset of fatigue during exercise and to restore homeostasis during recovery.
本综述描述了在高强度运动期间,收缩肌肉以高速率释放的钾离子([K⁺])和乳酸根离子浓度([Lac⁻])的分布过程。这导致收缩肌肉中间质和静脉血中的[K⁺]和[Lac⁻]增加。血浆中[K⁺]和[Lac⁻]大幅快速升高,导致这些离子转运至红细胞(RBC)内。这些离子分布于血液的血浆和RBC区室中的非收缩组织。非收缩组织从循环中摄取K⁺和Lac⁻,可显著减弱运动诱导的血浆中[K⁺]和[Lac⁻]升高。非收缩组织对血浆区室的这种明显调节作用,有助于维持有利于[K⁺]和[Lac⁻]从收缩肌肉的间质液净移动至微循环静脉侧的浓度梯度。这提供了如下条件:1)减少间质中[K⁺]的升高,从而降低肌膜去极化的幅度和速率;2)有利于Lac⁻从收缩肌细胞内进行肌膜转运,从而调节细胞内渗透压和H⁺浓度。运动停止后,恢复中的肌肉对K⁺的净摄取迅速,细胞内[K⁺]在3.5分钟内恢复90 - 95%,表明钠钾泵活性非常高。运动期间非收缩组织摄取的K⁺在恢复过程中可能会缓慢释放。在恢复的最初几分钟内,恢复中的肌肉继续向循环中释放Lac⁻,非收缩组织持续摄取Lac⁻长达30分钟。非收缩组织摄取Lac⁻导致细胞内[Lac⁻]升高。没有证据表明非收缩组织摄取的Lac⁻随后会释放;它可能在这些细胞内被代谢。我们得出结论,RBC和非收缩组织对K⁺和Lac⁻的摄取调节了血浆以及收缩肌肉的间质和细胞内区室中的离子稳态。这些调节过程有助于通过延迟运动期间疲劳的发生来维持活跃肌肉的功能,并在恢复过程中恢复稳态。