Dubouchaud H, Eydoux N, Granier P, Préfaut C, Mercier J
Laboratoire de Physiologie des Interactions, Service Central de Physiologie Clinique, Hôpital A de Villeneuve, 34295 Montpellier cedex 5, France.
J Appl Physiol (1985). 1999 Sep;87(3):955-61. doi: 10.1152/jappl.1999.87.3.955.
The effect of a single bout of exhaustive exercise on muscle lactate transport capacity was studied in rat skeletal muscle sarcolemmal (SL) vesicles. Rats were assigned to a control (C) group (n = 14) or an acutely exercised (E) group (n = 20). Exercise consisted of treadmill running (25 m/min, 10% grade) to exhaustion. SL vesicles purified from C and E rats were sealed because of sensitivity to osmotic forces. The time course of 1 mM lactate uptake in zero-trans conditions showed that the equilibrium level in the E group was significantly lower than in the C group (P < 0.05). The initial rate of 1 mM lactate uptake decreased significantly from 2.44 +/- 0.22 to 1.03 +/- 0.08 nmol. min(-1). mg protein(-1) (P < 0.05) after exercise, whereas that of 50 mM lactate uptake did not differ significantly between the two groups. For 100 mM external lactate concentration ([lactate]), exhaustive exercise increased initial rates of lactate uptake (219.6 +/- 36.3 to 465.4 +/- 80.2 nmol. min(-1). mg protein(-1), P < 0.05). Although saturation kinetics were observed in the C group with a maximal transport velocity of 233 nmol. min(-1). mg protein(-1) and a Michealis-Menten constant of 24.5 mM, saturation properties were not seen after exhaustive exercise in the E group, because initial rates of lactate uptake increased linearly with external [lactate]. We conclude that a single bout of exhaustive exercise significantly modified SL lactate transport activity, resulting in a decrease in 1 mM lactate uptake and was associated with alterations in the saturable properties at [lactate] above 50 mM. These results suggest that changes in sarcolemmal lactate transport activity may alter lactate and proton exchanges after exhaustive exercise.
在大鼠骨骼肌肌膜(SL)囊泡中研究了单次力竭运动对肌肉乳酸转运能力的影响。将大鼠分为对照组(C组,n = 14)或急性运动组(E组,n = 20)。运动方式为在跑步机上以25米/分钟、10%坡度的速度跑步直至力竭。由于对渗透压敏感,从C组和E组大鼠中纯化得到的SL囊泡被密封。零转运条件下1 mM乳酸摄取的时间进程表明,E组的平衡水平显著低于C组(P < 0.05)。运动后,1 mM乳酸摄取的初始速率从2.44±0.22显著降至1.03±0.08 nmol·min⁻¹·mg蛋白⁻¹(P < 0.05),而50 mM乳酸摄取的初始速率在两组之间无显著差异。对于100 mM的外部乳酸浓度([乳酸]),力竭运动增加了乳酸摄取的初始速率(从219.6±36.3增至465.4±80. .2 nmol·min⁻¹·mg蛋白⁻¹,P < 0.05)。虽然在C组中观察到饱和动力学,最大转运速度为233 nmol·min⁻¹·mg蛋白⁻¹,米氏常数为24. .5 mM,但在E组力竭运动后未观察到饱和特性,因为乳酸摄取的初始速率随外部[乳酸]呈线性增加。我们得出结论,单次力竭运动显著改变了SL乳酸转运活性,导致1 mM乳酸摄取减少,并与50 mM以上[乳酸]时可饱和特性的改变有关。这些结果表明,肌膜乳酸转运活性的变化可能会改变力竭运动后乳酸和质子的交换。