McKenna M J, Harmer A R, Fraser S F, Li J L
Department of Physical Education and Recreation, Victoria University of Technology, Footscray, Australia.
Acta Physiol Scand. 1996 Mar;156(3):335-46. doi: 10.1046/j.1365-201X.1996.199000.x.
Ionic regulation is critical to muscle excitation, contraction and metabolism, and thus for muscle function during exercise. This review focuses on the effects of training upon K+, Ca2+ and H+ ion regulation in muscle and K+ regulation in blood during exercise. Training enhances K+ regulation in muscle and blood and reduces muscular fatiguability. Endurance, sprint and strength training in humans induce an increased muscle Na+, K+ pump concentration, usually associated with a reduced rise in plasma [K+] during exercise. Although impaired muscle Ca2+ regulation plays a vital role in fatigue, little is known about possible training effects. In rat fast-twitch muscle, overload-induced hypertrophy and endurance training were associated with reduced sarcoplasmic reticulum Ca2+ uptake, consistent with fast-to-slow fibre transition. In human muscle, endurance and strength training had no effect on muscle Ca2+ ATPase concentration. Whilst muscle Ca2+ uptake, release and Ca2+ ATPase activity were depressed by fatigue, no differences were found between strength athletes and untrained individuals. Muscle H+ accumulation may contribute to fatigue during intense exercise and is also modified by sprint training. Sprint training may increase muscle Lac- and work output with exhaustive exercise, but the rise in muscle [H+] is unchanged or attenuated, indicating a reduced rise in muscle [H+] relative to work performed. Muscle buffering capacity can be dissociated from this improved H+ regulatory capacity after training. Thus, training enhances muscle and blood K+ and muscle H+ regulation during exercise, consistent with improved muscular performance and reduced fatiguability; however, little is known about training effects on muscle Ca2+ regulation during contraction.
离子调节对于肌肉的兴奋、收缩和代谢至关重要，因此对于运动期间的肌肉功能也很关键。本综述聚焦于训练对运动期间肌肉中钾离子（K⁺）、钙离子（Ca²⁺）和氢离子（H⁺）调节以及血液中钾离子调节的影响。训练可增强肌肉和血液中的钾离子调节，并降低肌肉疲劳性。人类的耐力训练、短跑训练和力量训练会导致肌肉中钠钾泵浓度增加，这通常与运动期间血浆中[K⁺]的升高幅度降低有关。尽管肌肉钙离子调节受损在疲劳中起着至关重要的作用，但关于可能的训练效果却知之甚少。在大鼠的快肌中，超负荷诱导的肥大和耐力训练与肌浆网钙离子摄取减少有关，这与纤维从快肌向慢肌的转变一致。在人类肌肉中，耐力训练和力量训练对肌肉钙离子ATP酶浓度没有影响。虽然疲劳会抑制肌肉钙离子摄取、释放以及钙离子ATP酶活性，但力量运动员和未经训练的个体之间未发现差异。在剧烈运动期间，肌肉氢离子积累可能导致疲劳，并且也会受到短跑训练的影响。短跑训练可能会在力竭运动时增加肌肉乳酸盐（Lac⁻）和功输出，但肌肉中[H⁺]的升高不变或减弱，这表明相对于所做的功，肌肉中[H⁺]的升高有所降低。训练后，肌肉缓冲能力可以与这种改善的氢离子调节能力相分离。因此，训练可增强运动期间肌肉和血液中的钾离子以及肌肉中的氢离子调节，这与肌肉性能改善和疲劳性降低相一致；然而，关于训练对收缩期间肌肉钙离子调节的影响却知之甚少。
