加州大学伯克利分校：乳酸不是运动员的毒药 耐力训练教会肌肉燃烧乳酸

Lactic Acid Not Athlete's Poison, But An Energy Source -- If You Know How To Use It

日期:2006年4月21日

来源:George Brooks 加州大学伯克利分校。

简介:

大多数运动员认为乳酸是他们的敌人，并且认为训练有助于消除他们肌肉中的代谢废物，这样肌肉可以持续运动更长的时间和更强壮。但是加州大学伯克利分校的生理学家乔治·布鲁克斯发现，训练实际上是在训练肌肉细胞使用乳酸作为燃料来获得更多的能量。通过训练，线粒体增加，通过一个穿梭机制吸收更多的乳酸，并燃烧它以产生更多的能量。

完整的故事

图示：一名学生志愿者在进行的间隙训练，研究剧烈运动期间的乳酸代谢

在马拉松运动员和极限运动员的知识中，乳酸是一种有毒物质，它会在肌肉中堆积，导致肌肉疲劳，降低性能和疼痛。

然而，加州大学伯克利分校(University of California, Berkeley) 30年的研究却得出了一个不同的结论: 乳酸可以成为你的朋友。

运动生理学家乔治·布鲁克斯(George Brooks)是加州大学伯克利分校的综合生物学教授，他说，教练和运动员都没有意识到这一点，但耐力训练教会我们的身体有效地利用乳酸作为燃料，与储存在肌肉组织中的碳水化合物和血液中的糖一样。有效地使用乳酸，或者乳酸盐，不仅可以防止乳酸的堆积，还能从身体的燃料中释放出更多的能量。

在一篇发表在1月的《美国生理学杂志-内分泌和新陈代谢》，布鲁克斯和他的同事们桥本武和Rajaa在加州大学巴克利分校的运动生理学实验室给乳酸故事加上了最后一张拼图，第一次把基于氧的有氧代谢和不需要氧的无氧代谢连接起来，以前认为有氧代谢和无氧代谢是独立的。

布鲁克斯说:“这是人们如何看待新陈代谢的根本变化。”“向我们展示了乳酸是氧化和糖酵解，或无氧代谢之间的联系。”

他和他的加州大学伯克利分校的同事们发现，肌肉细胞利用碳水化合物进行有氧代谢，产生乳酸作为副产品，然后用氧气燃烧乳酸，创造出更多的能量。第一个过程被称为糖酵解途径，在正常的运动过程中起主导作用，乳酸从肌肉细胞输出到血液中，被其他组织利用。然而，在剧烈运动过程中，第二次的上升会使快速积累的乳酸消除并产生更多的能量。

布鲁克斯说，训练可以帮助人们在累计到引起肌肉疲劳前清除乳酸，在细胞水平上，训练意味着在肌肉细胞中培养线粒体。线粒体——通常被称为细胞的动力来源——是乳酸被燃烧以获取能量的地方。

“世界上最好的运动员通过间歇训练（HIIT）来保持竞技状态”，布鲁克斯说，他指的是重复的短暂但剧烈的运动（HIIT)。“剧烈运动产生大的乳酸负荷，身体通过增加线粒体来适应快速利用乳酸。如果把它消耗掉，它就不会累积。

为了活动，肌肉需要产生ATP，三磷酸腺苷的形式的能量。大多数人认为葡萄糖是一种糖，它能提供这种能量，但在剧烈运动时，它的能量太少，速度也太慢，这迫使肌肉依赖糖原，这是一种储存在肌肉细胞内的碳水化合物。这两种燃料，都通过基本化学反应，产生ATP和产生乳酸，构成糖酵解途径，因为不需要氧气通常被称为无氧代谢。这一途径被认为是与基于氧的氧化途径，有时称为有氧代谢分开的，有氧代谢被用于在身体组织中燃烧乳酸和其他燃料。

在20世纪20年代，对死青蛙的实验似乎表明，乳酸的积累最终会导致肌肉停止工作。但在20世纪80年代和90年代布鲁克斯发现，在活着的、呼吸的动物中，乳酸从肌肉细胞中转移到血液中，并输送到不同的器官，包括肝脏，在那里它被氧气燃烧产生ATP。布鲁克斯发现，心脏甚至更喜欢乳酸作为燃料。

然而，布鲁克斯一直猜测，肌肉细胞本身可以重复使用乳酸盐，在过去10年的实验中，他发现了乳酸在线粒体内燃烧的证据，这是一个相互连接的管道网络，就像一个管道系统，在整个细胞质中都能到达。

例如，在1999年，他展示了耐力训练可以降低乳酸的血水平，即使细胞继续产生同样数量的乳酸。这意味着，某种程度上，细胞在训练过程中适应了，减少废物的排泄。他假设了一种“细胞内乳酸穿梭机制”，它可以从细胞质中运输乳酸，乳酸通过线粒体膜进入线粒体内部，在线粒体中乳酸被燃烧。在2000年，他展示了耐力训练增加了线粒体中乳酸转运分子的数量，显然是为了加速从细胞质中吸收乳酸进入线粒体进行燃烧。

这篇新论文和即将的第二篇论文就能提供直接证据，证明运输分子——乳酸穿梭通道（Lactate Shuttle)——和燃烧乳酸的酶之间的假设联系。事实上，细胞线粒体网络，或线粒体内质网，有一种蛋白质复合物，允许吸收和氧化，或燃烧乳酸。

布鲁克斯说:“这个实验证明乳酸是糖酵解代谢-分解碳水化合物的代谢和氧化代谢-利用氧气分解各种燃料的代谢之间的联系。”

博士后研究员Takeshi Hashimoto和员工研究助理Rajaa Hussien通过标记和显示乳酸通路的三个关键片段:乳酸转运蛋白;乳酸脱氢酶，催化乳酸转化为能量的第一步酶和线粒体细胞色素氧化酶，是使用氧气的蛋白质复合体。通过共聚焦显微镜观察骨骼肌细胞，两位科学家看到这些蛋白质聚集在线粒体内，附着在线粒体膜上，证明“细胞内乳酸穿梭通道”与线粒体中的酶直接相连，而线粒体内的酶与氧气一起燃烧。

布鲁克斯说:“我们的研究结果可以帮助运动员和训练师设计训练方案，同时避免过度训练，过多训练可能会杀死肌肉细胞。”“运动员们可能会本能地以一种建立线粒体的方式训练，但如果你永远不知道这种机制，你永远不知道你所做的是正确的事情。”这些发现重塑了对主要代谢途径的组织、功能和调控的基本思路。

布鲁克斯的研究得到了美国国立卫生研究院的支持。

故事来源: 加州大学伯克利分校提供的材料。

加州大学伯克利分校。“乳酸不是运动员的毒药，而是能量来源——如果你知道如何使用它的话。”《科学日报》。《科学日报》,2006年4月21日。。

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Lactic Acid Not Athlete's Poison, But An Energy Source -- If You Know How To Use It

Date:

April 21, 2006

Source:

University of California - Berkeley

Summary:

Most athletes consider lactic acid their enemy, and think that training helps eliminate the metabolic waste product from their muscles so the muscles will function longer and harder. But UC Berkeley physiologist George Brooks has found that training actually teaches muscle cells how to use lactic acid as a fuel to get more bang for the buck. With training, mitochondria grow, take in more lactate via a shuttle and burn it to generate more energy.

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FULL STORY

A student volunteers does interval training for a study of lactate metabolism during intense exercise. (George Brooks photo)

In the lore of marathoners and extreme athletes, lactic acid is poison, a waste product that builds up in the muscles and leads to muscle fatigue, reduced performance and pain.

Some 30 years of research at the University of California, Berkeley, however, tells a different story: Lactic acid can be your friend.

Coaches and athletes don't realize it, says exercise physiologist George Brooks, UC Berkeley professor of integrative biology, but endurance training teaches the body to efficiently use lactic acid as a source of fuel on par with the carbohydrates stored in muscle tissue and the sugar in blood. Efficient use of lactic acid, or lactate, not only prevents lactate build-up, but ekes out more energy from the body's fuel.

In a paper in press for the American Journal of Physiology - Endocrinology and Metabolism, published online in January, Brooks and colleagues Takeshi Hashimoto and Rajaa Hussien in UC Berkeley's Exercise Physiology Laboratory add one of the last puzzle pieces to the lactate story and also link for the first time two metabolic cycles - oxygen-based aerobic metabolism and oxygen-free anaerobic metabolism - previously thought distinct.

"This is a fundamental change in how people think about metabolism," Brooks said. "This shows us how lactate is the link between oxidative and glycolytic, or anaerobic, metabolism."

He and his UC Berkeley colleagues found that muscle cells use carbohydrates anaerobically for energy, producing lactate as a byproduct, but then burn the lactate with oxygen to create far more energy. The first process, called the glycolytic pathway, dominates during normal exertion, and the lactate seeps out of the muscle cells into the blood to be used elsewhere. During intense exercise, however, the second ramps up to oxidatively remove the rapidly accumulating lactate and create more energy.

Training helps people get rid of the lactic acid before it can build to the point where it causes muscle fatigue, and at the cellular level, Brooks said, training means growing the mitochondria in muscle cells. The mitochondria - often called the powerhouse of the cell - is where lactate is burned for energy.

"The world's best athletes stay competitive by interval training," Brooks said, referring to repeated short, but intense, bouts of exercise. "The intense exercise generates big lactate loads, and the body adapts by building up mitochondria to clear lactic acid quickly. If you use it up, it doesn't accumulate."

To move, muscles need energy in the form of ATP, adenosine triphosphate. Most people think glucose, a sugar, supplies this energy, but during intense exercise, it's too little and too slow as an energy source, forcing muscles to rely on glycogen, a carbohydrate stored inside muscle cells. For both fuels, the basic chemical reactions producing ATP and generating lactate comprise the glycolytic pathway, often called anaerobic metabolism because no oxygen is needed. This pathway was thought to be separate from the oxygen-based oxidative pathway, sometimes called aerobic metabolism, used to burn lactate and other fuels in the body's tissues.

Experiments with dead frogs in the 1920s seemed to show that lactate build-up eventually causes muscles to stop working. But Brooks in the 1980s and '90s showed that in living, breathing animals, the lactate moves out of muscle cells into the blood and travels to various organs, including the liver, where it is burned with oxygen to make ATP. The heart even prefers lactate as a fuel, Brooks found.

Brooks always suspected, however, that the muscle cell itself could reuse lactate, and in experiments over the past 10 years he found evidence that lactate is burned inside the mitochondria, an interconnected network of tubes, like a plumbing system, that reaches throughout the cell cytoplasm.

In 1999, for example, he showed that endurance training reduces blood levels of lactate, even while cells continue to produce the same amount of lactate. This implied that, somehow, cells adapt during training to put out less waste product. He postulated an "intracellular lactate shuttle" that transports lactate from the cytoplasm, where lactate is produced, through the mitochondrial membrane into the interior of the mitochondria, where lactate is burned. In 2000, he showed that endurance training increased the number of lactate transporter molecules in mitochondria, evidently to speed uptake of lactate from the cytoplasm into the mitochondria for burning.

The new paper and a second paper to appear soon finally provide direct evidence for the hypothesized connection between the transporter molecules - the lactate shuttle - and the enzymes that burn lactate. In fact, the cellular mitochondrial network, or reticulum, has a complex of proteins that allow the uptake and oxidation, or burning, of lactic acid.

"This experiment is the clincher, proving that lactate is the link between glycolytic metabolism, which breaks down carbohydrates, and oxidative metabolism, which uses oxygen to break down various fuels," Brooks said.

Post-doctoral researcher Takeshi Hashimoto and staff research associate Rajaa Hussien established this by labeling and showing colocalization of three critical pieces of the lactate pathway: the lactate transporter protein; the enzyme lactate dehydrogenase, which catalyzes the first step in the conversion of lactate into energy; and mitochondrial cytochrome oxidase, the protein complex where oxygen is used. Peering at skeletal muscle cells through a confocal microscope, the two scientists saw these proteins sitting together inside the mitochondria, attached to the mitochondrial membrane, proving that the "intracellular lactate shuttle" is directly connected to the enzymes in the mitochondria that burn lactate with oxygen.

"Our findings can help athletes and trainers design training regimens and also avoid overtraining, which can kill muscle cells," Brooks said. "Athletes may instinctively train in a way that builds up mitochondria, but if you never know the mechanism, you never know whether what you do is the right thing. These discoveries reshape fundamental thinking on the organization, function and regulation of major pathways of metabolism."

Brooks' research is supported by the National Institutes of Health.

Story Source:

Materials provided by University of California - Berkeley. Note: Content may be edited for style and length.

University of California - Berkeley. "Lactic Acid Not Athlete's Poison, But An Energy Source -- If You Know How To Use It." ScienceDaily. ScienceDaily, 21 April 2006. <www.sciencedaily.com/releases/2006/04/060420235214.htm>.