乳酸与运动表现:罪魁祸首还是有益之物?

Lactic acid and exercise performance : culprit or friend?

作者信息

Cairns Simeon P

机构信息

Institute of Sport and Recreation Research New Zealand, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand.

出版信息

Sports Med. 2006;36(4):279-91. doi: 10.2165/00007256-200636040-00001.

Abstract

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.

摘要

本文批判性地讨论了乳酸(实际上是乳酸盐和/或氢离子)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/氢离子浓度升高对骨骼肌收缩性能影响的研究历史悠久。表明乳酸/氢离子是罪魁祸首的证据一直基于相关性研究,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氢离子积累与力量下降之间密切的时间关系。此外,诱导酸中毒会损害未疲劳的人类或分离肌肉制剂中的肌肉收缩力,并提供了几种解释此类影响的机制。然而,最近一些备受瞩目的论文对“乳酸假说”提出了严重挑战。在二十世纪九十年代,这些发现主要涉及在较高的更接近生理的实验温度下,诱导酸中毒对去表皮或完整肌纤维的负面影响减弱。在二十一世纪初,最终表明乳酸对人工刺激激活的机械去表皮纤维几乎没有有害影响。也许更值得注意的是,现在有几份报告称,在分离的啮齿动物肌肉中,乳酸暴露或诱导酸中毒对钾缺乏的肌肉收缩有保护作用。此外,乳酸钠暴露可减轻原位刺激的大鼠肌肉中的严重疲劳,摄入乳酸钠可增加人类短跑时的疲劳时间。综上所述,这些最新发现导致了这样一种观点,即乳酸/氢离子在运动过程中具有促力作用。乳酸是损害运动表现的罪魁祸首,这一点不应被视为事实。对分离肌肉的实验表明,酸中毒在高强度运动期间几乎没有有害影响,甚至可能改善肌肉性能。相反,诱导酸中毒会加重全身动态运动期间的疲劳,而碱中毒可改善持续1至10分钟的运动项目中的运动表现。为了协调从分离的肌纤维到全身运动的研究结果,有人提出假设,人类严重的血浆酸中毒可能通过导致中枢神经系统对肌肉的驱动减少而损害运动表现。

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