Wang Y, Heigenhauser G J, Wood C M
Department of Biology, McMaster University, Hamilton, Ontario, Canada.
J Exp Biol. 1994 Oct;195:227-58. doi: 10.1242/jeb.195.1.227.
White muscle and arterial blood plasma were sampled at rest and during 4 h of recovery from exhaustive exercise in rainbow trout. A compound respiratory and metabolic acidosis in the blood was accompanied by increases in plasma lactate (in excess of the metabolic acid load), pyruvate, glucose, ammonia and inorganic phosphate levels, large elevations in haemoglobin concentration and haematocrit, red cell swelling, increases in the levels of most plasma electrolytes, but no shift of fluid out of the extracellular fluid (ECF) into the intracellular fluid (ICF) of white muscle. The decrease in white muscle pHi was comparable to that in pHe; both recovered by 4 h. Creatine phosphate and ATP levels were both reduced by 40% after exercise, the former recovering within 0.25 h, whereas the latter remained depressed until 4 h. Changes in creatine concentration mirrored those in creatine phosphate, whereas changes in IMP and ammonia concentration mirrored those in ATP. White muscle glycogen concentration was reduced 90% primarily by conversion to lactate; recovery was slow, to only 40% of resting glycogen levels by 4 h. During this period, most of the lactate and metabolic acid were retained in white muscle and there was excellent conservation of carbohydrate, suggesting that in situ glycogenesis rather than oxidation was the major fate of lactate. The redox state ([NAD+]/[NADH]) of the muscle cytoplasm, estimated from ICF lactate and pyruvate levels and pHi, remained unchanged from resting levels, challenging the traditional view of the 'anaerobic' production of lactate. Furthermore, the membrane potential, estimated from levels of ICF and ECF electrolytes using the Goldman equation, remained unchanged throughout, challenging the view that white muscle becomes depolarized after exhaustive exercise. Indeed, ICF K+ concentration was elevated. Lactate was distributed well out of electrochemical equilibrium with either the membrane potential (Em) or the pHe-pHi difference, supporting the view that lactate is actively retained in white muscle. In contrast, H+ was actively extruded. Ammonia was distributed passively according to Em rather than pHe-pHi throughout recovery, providing a mechanism for retaining high ICF ammonia levels for adenylate resynthesis in situ. Although lipid is not traditionally considered to be a fuel for burst exercise, substantial decreases in free carnitine and elevations in acyl-carnitines and acetyl-CoA concentrations indicated an important contribution of fatty acid oxidation by white muscle during both exercise and recovery.
在虹鳟鱼静息状态以及从力竭运动中恢复4小时的过程中，采集了白肌和动脉血浆样本。血液中出现复合性呼吸性和代谢性酸中毒，同时血浆乳酸（超过代谢性酸负荷）、丙酮酸、葡萄糖、氨和无机磷酸盐水平升高，血红蛋白浓度和血细胞比容大幅升高，红细胞肿胀，大多数血浆电解质水平升高，但没有液体从细胞外液（ECF）转移到白肌的细胞内液（ICF）中。白肌细胞内pH值（pHi）的下降与细胞外pH值（pHe）的下降相当；两者在4小时内均恢复。运动后肌酸磷酸和ATP水平均降低了40%，前者在0.25小时内恢复，而后者直到4小时仍处于较低水平。肌酸浓度的变化与肌酸磷酸的变化一致，而肌苷酸（IMP）和氨浓度的变化与ATP的变化一致。白肌糖原浓度主要通过转化为乳酸而降低了90%；恢复缓慢，到4小时时仅恢复到静息糖原水平的40%。在此期间，大部分乳酸和代谢性酸保留在白肌中，碳水化合物保存良好，这表明乳酸的主要命运是在原位进行糖原异生而非氧化。根据ICF乳酸和丙酮酸水平以及pHi估算的肌细胞质氧化还原状态（[NAD+]/[NADH]）与静息水平相比没有变化，这对传统的乳酸“无氧”产生观点提出了挑战。此外，使用戈德曼方程根据ICF和ECF电解质水平估算的膜电位在整个过程中保持不变，这对力竭运动后白肌会去极化的观点提出了挑战。事实上，ICF钾离子浓度升高。乳酸的分布与膜电位（Em）或pHe - pHi差值均处于电化学不平衡状态，这支持了乳酸在白肌中被主动保留的观点。相比之下，氢离子被主动排出。在整个恢复过程中，氨根据Em而非pHe - pHi被动分布，这为在原位保留高ICF氨水平以进行腺苷酸再合成提供了一种机制。尽管传统上不认为脂质是爆发性运动的燃料，但游离肉碱的大幅减少以及酰基肉碱和乙酰辅酶A浓度的升高表明，白肌在运动和恢复过程中脂肪酸氧化起到了重要作用。
