Lindinger M I, Heigenhauser G J
School of Human Biology, University of Guelph, Ont., Canada.
Can J Physiol Pharmacol. 1991 Feb;69(2):246-53. doi: 10.1139/y91-038.
Intense muscle contractions result in large changes in the intracellular concentrations of electrolytes. The purpose of this study was to examine the contributions of changes in intracellular strong ions to calculated changes in steady-state membrane potential (Em) and muscle intracellular H+ concentration ([H+]i). A physicochemical model is used to examine the origin of the changes in [H+]i during intense muscle contraction. The study used the isolated perfused rat hindlimb intermittently stimulated to contract at high intensity for 5 min. This resulted in significant K+ depletion of both slow (soleus) and fast (white gastrocnemius, WG) muscle fibers and a release of K+ and lactate (Lac-) into venous perfusate. The major contributor to a 12- to 14-mV depolarization of Em in soleus and WG was the decrease in intracellular K+ concentration ([K+]i). The major independent contributors to [H+]i are changes in the concentrations of strong and weak ions and in CO2. Significant decreases in the strong ion difference [( SID]i) in both soleus and WG contributed substantially to the increase in [H+]i during stimulation. In WG the model showed that the decrease in [SID]i accounted for 35% of the increase in [H+]i (133-312 nequiv/L; pHi = 6.88-6.51) at the end of stimulation. Of the main contributors to decreased [SID]i, increased [Lac-]i and decreased [K+]i contributed 40 and 60%, respectively, to increased [H+]i, whereas a decrease in [PCr2-]i contributed to reduced [H+]i. It is concluded that decreased muscle [K+]i during intense contractions is the single most important contributor to reduced Em and increased [H+]i. Depletion of PCr2- simultaneous to the changes in [Lac-]i and [K+]i prevents larger increases in [H+]i and helps maintain the intracellular acid-base state.
强烈的肌肉收缩会导致细胞内电解质浓度发生巨大变化。本研究的目的是探讨细胞内强离子变化对稳态膜电位（Em）和肌肉细胞内H⁺浓度（[H⁺]i）计算变化的贡献。采用物理化学模型研究强烈肌肉收缩期间[H⁺]i变化的起源。该研究使用离体灌注的大鼠后肢，间歇性高强度刺激使其收缩5分钟。这导致慢肌（比目鱼肌）和快肌（白腓肠肌，WG）纤维中的K⁺显著耗竭，并使K⁺和乳酸（Lac⁻）释放到静脉灌注液中。比目鱼肌和WG中Em去极化12至14 mV的主要原因是细胞内K⁺浓度（[K⁺]i）降低。[H⁺]i的主要独立影响因素是强离子和弱离子浓度以及CO₂的变化。比目鱼肌和WG中强离子差[（SID）i]的显著降低在很大程度上导致了刺激期间[H⁺]i的增加。在WG中，模型显示刺激结束时[SID]i的降低占[H⁺]i增加量（133 - 312 nmol/L；pH i = 6.88 - 6.51）的35%。在导致[SID]i降低的主要因素中，[Lac⁻]i增加和[K⁺]i降低分别导致[H⁺]i增加40%和60%，而[PCr²⁻]i降低则导致[H⁺]i降低。研究得出结论，强烈收缩期间肌肉[K⁺]i降低是Em降低和[H⁺]i增加的最重要单一因素。与[Lac⁻]i和[K⁺]i变化同时发生的PCr²⁻耗竭可防止[H⁺]i进一步大幅增加，并有助于维持细胞内酸碱状态。
