IELTS Academic Reading Practice Test 317

At the end of the nineteenth century, yellow fever was the most feared disease of the American tropics. An infection that damages the liver and kidneys, it began with fever and headache, turned the skin and the whites of the eyes yellow, and in severe cases ended in black vomiting and death. In Havana, the Cuban capital occupied by United States forces after the Spanish-American War of 1898, the disease appeared every summer. It killed soldiers and civilians alike, and it alarmed the officers responsible for the health of the army, because a single case could empty a barracks.

Most doctors blamed 'miasma', the foul air thought to rise from refuse, or 'fomites', the bedding and clothing of the sick, which were believed to hold the infection and carry it from place to place. Quarantine against infected belongings was a standard response. A minority view existed. In 1881 a Cuban physician, Carlos Finlay, told an international sanitary conference in Washington that yellow fever was transmitted by a particular mosquito, a species now known as Aedes aegypti. Finlay had experimented for years, but he could not produce a convincing number of cases in volunteers, and his claim was largely dismissed.

In 1900 the Surgeon General, George Miller Sternberg, appointed a board to investigate the disease in Cuba. Its head was Walter Reed, an army surgeon from Virginia who had qualified in medicine while still in his teens and had spent much of his career in remote frontier posts before becoming a professor of bacteriology in Washington. The other members were James Carroll, a bacteriologist, Jesse Lazear, a young physician who had studied in Germany, and Aristides Agramonte, a Cuban-born doctor who had survived an attack of the fever and was therefore assumed to be immune.

The board began by reviewing Finlay's work. In the summer of 1900 it carried out experiments in which mosquitoes that had fed on patients in the fever wards were allowed to bite healthy volunteers, most of them young soldiers or recent Spanish immigrants. Carroll was bitten and fell dangerously ill; he recovered, but the illness damaged his heart for the rest of his life. Lazear was bitten in September and died within days, at the age of thirty-four.

Reed was shaken but not deterred. In November 1900, with money from the army, he built a small camp outside Havana and named it Camp Lazear in his colleague's memory. It consisted of two wooden huts, and it was designed to settle the argument between the mosquito and the fomite once and for all. In one hut, volunteers slept in bedding and wore clothing taken from patients who had died of the fever, and the hut was carefully protected against insects. In the other, they slept in clean bedding but shared the space with mosquitoes that had fed on the sick.

The results were unambiguous. The men who slept among the contaminated sheets and clothes did not fall ill, even though the hut was deliberately kept hot and airless to concentrate any supposed infection. Those who were bitten did. Reed reported the board's findings in 1901, arguing that the fever passed from person to person only through the mosquito and that a patient could not infect anyone else directly. A mosquito, he calculated, became capable of transmitting the disease about twelve days after feeding on an infected person, and remained so for the rest of its life.

What is often overlooked is how the board obtained its volunteers. Reed drew up a contract, printed in Spanish and English, which set out the risks, the payment offered and the arrangements for medical care. Volunteers, many of them poor and hoping for the money, signed it or made a mark. The document is often cited as an early example of informed consent, though by modern standards it would hardly pass: the sums were large enough to be a strong inducement, and nobody checked whether the volunteers had understood the danger.

The board's conclusions were not universally welcomed. Some senior medical figures in the United States continued to defend the old theories for years, and Reed himself was cautious in public. The practical consequence, however, came quickly. Major William Gorgas, the chief sanitary officer in Havana, attacked the insects rather than the filth: standing water was drained or covered with oil, cisterns were sealed and houses were fumigated. Within a few months yellow fever had almost vanished from a city in which it had been endemic for generations.

Gorgas took the same methods to Panama, where an earlier French attempt to build a canal had collapsed, in part because of the disease. The American effort succeeded where the French had failed, and the campaign against the mosquito is usually counted, alongside the engineering, among the reasons. Reed did not live to see the canal. He died in November 1902, after an operation for appendicitis, at the age of fifty-one.

The cause of the disease, a virus, was not identified until the late 1920s, and a vaccine followed in the 1930s. Reed's board had therefore been right about the route of transmission without ever knowing what travelled along it. Finlay, who had argued his case for two decades before the board was appointed, is now honoured in Cuba as the man who first pointed at the mosquito, while Reed is commemorated in the United States, where the army's medical research institute still bears his name.

Lifting a weight that felt heavy in January may feel easy by March. Part of the improvement is a matter of skill: the brain learns to activate the muscle more completely. Part of it is a matter of tissue: the muscle itself becomes larger and stronger. Coaches often speak of 'gaining muscle' as though it were a single process, but the two adaptations happen on different timetables, and confusion between them explains many of the arguments that surround training advice. Gains in strength arrive within days; real growth in the tissue accumulates over months.

Skeletal muscle is built from long cells called fibres, each containing bundles of protein filaments. The filaments are arranged in repeating units known as sarcomeres, where threads of myosin pull on threads of actin, shortening the unit and generating force. A single fibre contains many thousands of sarcomeres, and it is the total number of these units, together with the thickness of the filaments, that largely determines how much force a muscle can produce. Growth in size, known as hypertrophy, therefore means adding protein filaments; the number of fibres appears to be fixed in adulthood. Fibres also differ in type, from slow fibres that resist fatigue to fast fibres that produce rapid, powerful contractions.

In the first weeks of a training programme, strength can rise by a substantial margin while the muscle shows little or no change in size. This early improvement is usually attributed to the nervous system. The brain recruits more motor units, the bundles of fibres controlled by a single nerve cell, and fires them more rapidly and in a better-coordinated sequence. Studies in which only one limb is trained have found modest strength gains in the untrained limb, an effect known as cross-education, which cannot be explained by growth in the muscle itself. Beginners often notice the difference long before anyone else can see it.

Once a muscle is subjected to repeated high tension, a cascade of chemical signals is set off inside the fibres. The best known of these pathways involves a protein called mTOR, which acts as a switch for the manufacture of new muscle protein. After a single session of resistance exercise, protein synthesis in the trained muscle can remain elevated for a day or more. What the cell actually senses is still debated: candidates include the stretching of structural proteins, the depletion of energy stores and the movement of calcium. The tension itself, rather than the work done, appears to be the critical stimulus, which is why heavy loads are so effective.

Muscle fibres are unusual among body cells in carrying many nuclei, and a fibre can grow only so far before it needs more. Exercise activates satellite cells, dormant cells that sit on the surface of the fibre, which divide and donate their nuclei to it. Without a sufficient supply of these nuclei, a fibre cannot sustain further growth. The idea that muscles must be damaged and then repaired in order to grow is widely repeated in gyms, but the evidence is less clear: growth occurs after training that causes little measurable damage, and severe damage may hinder rather than help.

Protein supplies the amino acids from which new muscle protein is made, and the total amount eaten over a day matters more than the precise timing of meals. Most researchers suggest roughly 1.6 grams of protein per kilogram of body weight per day for people who train seriously, and intakes above that appear to produce little extra benefit. Spreading protein across three or four meals, each containing a source rich in the amino acid leucine, seems to stimulate synthesis more effectively than a single large serving in the evening. Supplements are convenient, but food appears to work just as well.

Testosterone and growth hormone are both released in response to hard exercise, and both have been assumed to drive growth. Their importance is easily overstated. Testosterone does contribute, but the short-lived rise after a workout is small compared with the normal daily variation. Growth hormone, despite its name, appears to have little direct effect on muscle size in adults; people who produce too much of it develop other medical problems rather than unusually large muscles. Hormone levels measured after a workout therefore reveal little about long-term growth.

Muscle is expensive tissue to maintain, and the body sheds it when it is not used. Immobilisation after an injury, or a few weeks without training, reduces both strength and size, with strength usually falling first. Yet the loss is not complete. Detraining also affects the nervous system, which loses some of its fine control. Fibres that have gained nuclei appear to keep them for years, which may explain why retrained muscle recovers faster than muscle built for the first time. This is the cellular basis of what athletes call muscle memory.

How much a given person gains from a given programme varies enormously. In controlled trials, some participants add considerable muscle on a standard routine while others, following exactly the same routine, add almost none. Part of this is genetic, part may be a matter of sleep, diet and recovery, and part remains unexplained. Researchers also point out that measuring muscle growth accurately in living people is difficult, and that many studies rely on small numbers of young, healthy men. Even the word growth is defined differently in different laboratories, which makes comparisons between studies hazardous.

Plasma is the pale liquid in which blood cells float, and it is the raw material for a growing range of medicines. Antibodies concentrated from plasma are used to treat immune deficiencies and to protect people whose immune systems are damaged; clotting factors keep haemophiliacs alive; other proteins treat burns and rare inherited disorders. Demand has risen steadily for decades, and every dose begins with a needle in someone's arm. Unlike a chemical drug, plasma cannot be manufactured; it can only be given. That fact turns a technical question into a moral one: should the people who provide it be paid?

Collecting plasma takes longer than giving whole blood. A machine draws blood, separates the plasma and returns the cells to the donor, a cycle repeated several times over perhaps forty minutes. Because the cells are returned, plasma donors can give far more often than whole-blood donors, in some countries as often as twice a week. The plasma is then pooled and processed in large plants, where it is split into its constituent proteins in a procedure known as fractionation. A single pool may combine thousands of donations, which makes the safety of every donor matter to hundreds of patients.

Most high-income countries collect blood for transfusion from volunteers who receive nothing but refreshments and thanks. The World Health Organization supports this model, recommending that all countries move towards voluntary, non-remunerated donation. The reason is partly historical. In the 1960s and 1970s, studies in the United States found higher rates of hepatitis in blood bought from paid donors than in blood freely given, and the United States itself moved towards an all-volunteer supply for transfusion. The lesson drawn was that people who sell their blood have an incentive to conceal illness or to donate more often than is safe.

The classic statement of this view is a book published in 1970 by the British social scientist Richard Titmuss, The Gift Relationship. Titmuss compared the blood systems of Britain and the United States and argued that treating blood as a commodity changes the relationship between donor and patient and erodes the sense of obligation that holds a health service together. He contended that a market would attract the wrong donors, increase costs and lower quality. The book became a standard reference for those who defend unpaid donation.

Yet the argument has an awkward consequence. Countries that refuse to pay their own donors often import plasma products from countries that do pay them. Several European states, including Germany and Austria, permit payment for plasma collected for manufacturing, and the United States, where donors are commonly paid, supplies a large share of the plasma traded internationally. A British or Canadian patient treated with a plasma-derived medicine may therefore be benefiting from payments that the patient's own health system considers unacceptable. Critics call this hypocrisy; defenders reply that importing is a pragmatic compromise while domestic collection grows.

The safety objection is also weaker than it once was. Since the 1980s, screening of donors, testing of every donation for viruses and, above all, methods for inactivating viruses during manufacture have transformed the risk. Modern fractionation includes steps, among them heat treatment, solvent-detergent washing and filtration, that destroy or remove infectious agents. A paid donor is not, in itself, a dangerous donor. What matters is whether the collection system tests thoroughly and can trace a product back to the person who gave it.

Evidence about incentives is more interesting than either side usually admits. Field experiments have produced mixed results: modest rewards sometimes increase donations and sometimes reduce them, and the effect depends on how the offer is framed. When a payment is presented as the price of a product, some donors appear to lose the sense that they are making a gift and stay away; when the same sum is presented as a token of thanks for time and travel, it may be welcomed. Economists call this crowding out, and it warns against assuming that a bigger reward always produces more blood.

The exploitation objection is harder to dismiss. Plasma is bought overwhelmingly from people who need money, and in some cities paid collection centres cluster in poor neighbourhoods. Frequent donation can lower levels of antibodies, and if iron is not monitored it may contribute to anaemia; the long-term effects of very frequent plasma donation are still being studied. Against this, defenders point out that the transaction is voluntary, that donors are paid for their time rather than for a body part, and that the money may be the reason a student finishes a course or a parent pays a bill.

The choice, then, may not be between payment and purity but between different kinds of payment. A regulated system can cap how often a person donates, require independent medical checks, insist that donors understand the risks and prevent brokers from recruiting aggressively. Compensation for time and travel, paid to everyone regardless of income, is easier to defend than a market in which the poorest sell most. Some countries have already moved in this direction for plasma while keeping whole blood unpaid.

My own view is that outright purchase, left to the market, is difficult to justify, but that a tightly regulated scheme of compensation for plasma donors is defensible and probably necessary. Plasma is not a spare part to be sold; neither is it so sacred that patients should wait for it. The test of any system is whether it protects the health of the donor as carefully as the life of the recipient, and whether the choice to give is genuinely free.