Lactic acid and exercise performance - Culprit or friend?
Lactic acid and exercise performance - Culprit or friend?
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DOI：
10.2165/00007256-200636040-00001
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发表时间：
2006-01-01
期刊：
影响因子：
9.8
通讯作者：
Cairns, SP
中科院分区：
文献类型：
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作者：
Cairns, SP
本文批判性地讨论了乳酸或实际上的乳酸和/或氢 (H+) 离子的积累是否是骨骼肌疲劳的主要原因，即肌肉力量或功率输出下降导致运动表现受损。关于肌肉或血浆中乳酸/H+浓度增加对骨骼肌收缩性能的影响的研究已有很长的历史。表明乳酸/H+ 是罪魁祸首的证据基于相关型研究，这些研究揭示了青蛙、啮齿动物或人类肌肉疲劳刺激期间肌内乳酸或 H+ 积累与力量下降之间的密切时间关系。此外，诱发的酸中毒会损害非疲劳人类或分离的肌肉制剂的肌肉收缩性，并且已经提供了几种解释这种影响的机制。然而，最近一些备受瞩目的论文严重挑战了“乳酸假说”。在 20 世纪 90 年代，这些发现主要涉及在更高、更生理的实验温度下，减少去皮或完整肌肉纤维中诱发酸中毒的负面影响。 2000 年代初，研究结果表明，乳酸对人工刺激激活的机械结皮纤维几乎没有有害影响。也许更值得注意的是，现在有几份报告表明，乳酸暴露或诱发酸中毒对离体啮齿动物肌肉中钾抑制的肌肉收缩有保护作用。此外，接触乳酸钠可以减轻原位刺激的大鼠肌肉的严重疲劳，并且摄入乳酸钠可以增加人类短跑期间的力竭时间。总而言之，这些最新发现得出了乳酸/H+在运动过程中具有增效作用的观点。不应将乳酸视为损害运动表现的异常物质。对孤立肌肉的实验表明，酸中毒几乎没有有害影响，甚至可以改善高强度运动期间的肌肉表现。相反，诱发性酸中毒会加剧全身动态运动时的疲劳，而碱中毒则可以提高持续 1-10 分钟的运动表现。为了将孤立肌纤维的研究结果与全身运动相协调，假设人类严重的血浆酸中毒可能会导致中枢神经系统对肌肉的驱动力减弱，从而损害运动表现。
This article critically discusses whether accumulation of lactic acid, or in reality lactate and/or hydrogen (H+) ions, is a major cause of skeletal muscle fatigue, i.e. decline of muscle force or power output leading to impaired exercise performance. There exists a long history of studies on the effects of increased lactate/H+ concentrations in muscle or plasma on contractile performance of skeletal muscle. Evidence suggesting that lactate/H+ is a culprit has been based on correlation-type studies, which reveal close temporal relationships between intramuscular lactate or H+ accumulation and the decline of force during fatiguing stimulation in frog, rodent or human muscle. In addition, an induced acidosis can impair muscle contractility in non-fatigued humans or in isolated muscle preparations, and several mechanisms to explain such effects have been provided. However, a number of recent high-profile papers have seriously challenged the 'lactic acid hypothesis'. In the 1990s, these findings mainly involved diminished negative effects of an induced acidosis in skinned or intact muscle fibres, at higher more physiological experimental temperatures. In the early 2000s, it was conclusively shown that lactate has little detrimental effect on mechanically skinned fibres activated by artificial stimulation. Perhaps more remarkably, there are now several reports of protective effects of lactate exposure or induced acidosis on potassium-depressed muscle contractions in isolated rodent muscles. In addition, sodium-lactate exposure can attenuate severe fatigue in rat muscle stimulated in situ, and sodium lactate ingestion can increase time to exhaustion during sprinting in humans. Taken together, these latest findings have led to the idea that lactate/ H+ is ergogenic during exercise.It should not be taken as fact that lactic acid is the deviant that impairs exercise performance. Experiments on isolated muscle suggest that acidosis has little detrimental effect or may even improve muscle performance during high-intensity exercise. In contrast, induced acidosis can exacerbate fatigue during whole-body dynamic exercise and alkalosis can improve exercise performance in events lasting 1-10 minutes. To reconcile the findings from isolated muscle fibres through to whole-body exercise, it is hypothesised that a severe plasma acidosis in humans might impair exercise performance by causing a reduced CNS drive to muscle.