医学考博英语阅读 | 锻炼与长寿

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Science and technology：Exercise and longevity

Worth all the sweat

Just why exercise is so good for people is, at last, being understood

ONE sure giveaway of quack medicine is the claim that a product can treat any ailment. There are, sadly, no panaceas. But some things come close, and exercise is one of them. As doctors never tire of reminding people, exercise protects against a host of illnesses,from heart attacks and dementia to diabetes and infection. How it does so, however, remains surprisingly mysterious. But a paper just published in Nature by Beth Levine of the University of Texas Southwestern Medical Centre and her colleagues sheds some light on the matter.

Dr Levine and her team were testing a theory that exercise works its magic, at least in part, by promoting autophagy. This process, whose name is derived from the Greek for self-eating, is a mechanism by which surplus, worn-out or malformed proteins and other cellular components are broken up for scrap and recycled.

To carry out the test, Dr Levine turned to those stalwarts of medical research, genetically modified mice. Her first batch of rodents were tweaked so that their autophagosomes, structures that form around components which have been marked for recycling—glowed green. After these mice had spent half an hour on a treadmill, she found that the number of autophagosomes in their muscles had increased, and it went on increasing until they had been running for 80 minutes.

To find out what, if anything, this exercise-boosted autophagy was doing for mice, the team engineered a second strain that was unable to respond this way. Exercise, in other words, failed to stimulate their recycling mechanism. When this second group of modified mice were tested alongside ordinary ones, they showed less endurance and had less ability to take up sugar from their bloodstreams.

There were longer-term effects, too.

In mice, as in people, regular exercise helps prevent diabetes. But when the team fed their second group of modified mice a diet designed to induce diabetes, they found that exercise gave no protection at all.

Dr Levine and her team reckon their results suggest that manipulating autophagy may offer a new approach to treating diabetes. And their research is also suggestive in other ways. Autophagy is a hot topic in medicine, as biologists have come to realise that it helps protect the body from all kinds of ailments. The virtues of recycling autophagy is an ancient mechanism, shared by all eukaryotic organisms. It probably arose as an adaptation to scarcity of nutrients. Critters that can recycle parts of themselves for fuel are better able to cope with lean times than those that cannot.

But over the past couple of decades, autophagy has also been shown to be involved in things as diverse，as fighting bacterial infections and slowing the onset of neurological conditions like Alzheimer's and Huntington's diseases. Most intriguingly of all, it seems that it can slow the process of ageing. Biologists have known for decades that feeding animals near-starvation diets can boost their lifespans dramatically. Dr Levine was a member of the team which showed that an increased level of autophagy, brought on by the stress of living in a constant state of near-starvation, was the mechanism responsible for this life extension.

The theory is that what are being disposed of in particular are worn-out mitochondria. These structures are a cell's power-packs. They are where glucose and oxygen react together to release energy.

Such reactions, though, often create damaging oxygen-rich molecules called free radicals, which are thought to be one of the driving forces of ageing. Getting rid of wonky mitochondria would reduce free-radical production and might thus slow down ageing.

A few anti-ageing zealots already subsist on near-starvation diets, but Dr Levine's results suggest a similar effect might be gained in a much more agreeable way, via vigorous exercise.

The team's next step is to test whether boosted autophagy can indeed explain the life-extending effects of exercise. That will take a while. Even in animals as short-lived as mice, she points out, studying ageing is a long-winded process. But she is sufficiently confident about the outcome that she has, in the meantime, bought herself a treadmill.

科学技术：锻炼与长寿

出点汗，值了！

为什么锻炼有利于身体健康呢，人们终于知道答案了

有一种绝对能推销出去狗皮膏药的方法就是说它包治百病。遗憾的是灵丹妙药并不存在。但有些方法却起到类似的作用，锻炼就是其中之一。医生们一直不厌其烦地提醒人们锻炼身体有助于防范一系列疾病，包括心脏病、痴呆症、糖尿病以及感染。但是人们一直不知道为什么。德克萨斯大学西南医学中心贝丝莱文及其同事最近在《自然》杂志发表的论文给出了一些解释。

莱文博士及其小组证明一个理论的正确性，即锻炼之所以有神奇的作用，部分原因是它能促进自体吞噬。这个名称来自希腊词语自食其肉，指的是多余的、不能再用的、畸形的蛋白质和其他细胞成分被分解成碎片并再循环。

莱文博士在这个实验中使用转基因老鼠作为实验对象，医学研究中经常使用转基因老鼠。第一组老鼠被调整使得其细胞中的自噬体发出绿光，这种结构形成的部分被用于再循环。这些老鼠被放在跑步机上半个小时后，莱文博士发现它们肌肉中的自噬体增加了，直到跑了80分钟才停止增加。

为了找出这种由锻炼刺激的自噬作用对老鼠有什么作用，研究小组设计了另一组不能如此反应的老鼠。换句话说，锻炼并没刺激再循环机制。当第二组的转基因老鼠和普通老鼠一起接受实验时，它们的耐力逊于后者，也不能很好地从血液中吸收糖分。

还有长期影响。

老鼠和人一样，定期锻炼有助于预防糖尿病。 但是在研究小组给第二组转基因老鼠喂了一种专门用来诱发糖尿病的食物后，他们发现锻炼并没有任何预防效果。

莱文博士及其小组认为实验结果表明受到操纵的自噬作用有可能提供一种新的治疗糖尿病的方法。他们的研究在其他方面也有启示。

自噬作用在医学界是个热门话题，因为生物学家逐渐意识到它能抵御各种小病。再循环的功效自体吞噬机制很古老，所有真核生物都有。它的产生可能是为了适应营养物质的缺乏的环境。有些家畜能循环利用它们身体的一部分作为养料，这样的动物比其他的动物在食物匮乏期更容易生存。

但是在过去几十年里，自体吞噬在其他很多地方也有所体现，比如对抗细菌感染、放缓老年痴呆症和亨丁顿舞蹈症等神经症状的发病。

最有趣的是，看起来它还延缓了老化过程。生物学家几十年来都知道在动物保持接近饥饿的状态下喂食能大幅度提高它们的寿命。莱文博士曾经工作的一个小组证明在长期接近饥饿的状态下生存的压力引起了自体吞噬水平的提高，这种原理使得寿命延长。

被处理掉的其实是衰弱的线粒体。这种结构给细胞提供能量。在线粒体里，葡萄糖和氧气共同作用释放能量。不过这种反应却常常制造出有害的富氧分子，即自由基，它是促成老化的原因之一。除掉没用的线粒体可以减少自由基的生成，这样就可能减缓老化过程。

一些反老化的狂热分子已经开始靠保持饥饿状态的饮食为生了，但是莱文博士的实验结果表示通过积极锻炼身体这样一种更随和的方式也能得到类似的效果。

该小组下一步将测试被激发的自体吞噬是否真的能解释锻炼有助于长寿。这尚需时间方能出结果。她指出即使研究像老鼠这样寿命很短的动物也是长期曲折的过程。但是她对结果非常自信，于此同时还给自己也买了一个跑步机。

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医学考博英语阅读 | 治疗自闭症

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