A  For people confined to bed for long periods of time, or for astronauts in microgravity, muscle wasting is a serious problem. Wasting, or atrophy, is a symptom not only of disuse and injury, but of many diseases, including kidney failure, cancer and AIDS. Once enough muscle has been lost, a vicious cycle sets in as exercise becomes increasingly difficult, which in turn leads to disuse and further atrophy.

B  Despite more than three decades of research into alternatives, the only way to stop such patients losing muscle is a long course of physiotherapy involving weight-bearing exercise, but this is of little use to the weakest and sickest — and in most cases, starts only after wasting has already set in. The use of anabolic steroids is being explored for some conditions. But these compounds have a huge range of effects on the body besides promoting muscle growth, some of them undesirable, and only appear to work well in conjunction with exercise.

C  Alfred Goldberg, a cell biologist at Harvard University, began studying muscle atrophy in the late 1960s. What he and others discovered was that, rather than being a passive side effect of disuse or disease, muscle wasting is an active process controlled by a complex genetic pathway. So, if someone found out how it was turned on, it ought to be possible to turn it off. 'Back then we didn't know the pathway for muscle breakdown,' says Goldberg, 'but about five years ago our work showed that no matter what the trigger — disuse, metabolic disease or fasting — the same biochemical programme is responsible.'

D  The process involves the ubiquitin-proteasome pathway (UPP), the disposal machinery used to break down unwanted proteins in the cell (New Scientist, 17 December 2005, p. 36). Once the system has been activated, ubiquitin 'destroy me' labels are added to muscle proteins. This breaks down the muscle filaments within cells, but does not change the number of muscle cells. Instead, they become thinner and weaker. Further studies showed that at least 90 genes are involved in atrophy; Goldberg calls them 'atrogenes.' Although it is still unknown which of these genes triggers atrophy, it soon became clear that two of them are essential to the process. Atrogin1 and muRF1 were first described in 2001 and are the only two atrogenes active only during muscle atrophy. They code for ubiquitin ligases, the enzymes that attach the 'destroy me' labels to proteins. The genes are barely active in normal muscle, but expression levels shoot up in sick animals. Knock out either, and muscle wasting all but stops.

E  An experiment was conducted on a 'superboy' who was normal at birth, lacking fat; by the age of five, he was excellent at weightlifting, lifting as much as three kilograms. The scientists found that this is closely related to his mother, who is a professional runner, and that his extended family has unusually strong abilities. Doctors later found that the boy had a mutation in the gene that produces myostatin, a protein that normally limits muscle growth. But the drug can have a temporary effect.

F  There are still many gaps to be filled in, but those in the field agree that the question is no longer if we can develop anti-wasting treatments, but when. As researchers close in on this target, excitement is mounting about exactly what such treatments could achieve. Patients due to be confined to bed for more than a few days could be given the drug as soon as they begin bed rest to prevent muscle loss that would otherwise slow their recovery. Weaning patients off respirators would become easier as doctors could prevent wasting of the diaphragm. Disease need no longer lead to weakness, and broken bones would not mean long and painful physiotherapy sessions to rebuild muscle strength. And since loss of muscle mass is a major reason why we grow frail with age, an anti-wasting drug could keep older people on their feet and living independently for longer.

G  The prospect of preventing atrophy is also of great interest to NASA, particularly in view of its much talked-about mission to Mars. By the time astronauts reach the Red Planet, they can expect to lose up to 25 per cent of their muscle mass and be too weak to walk, let alone put on a space suit and carry out repairs. That is why Goldberg's work is funded by the National Space Biomedical Research Institute in Houston, Texas, set up by NASA.

H  While there are valid medical and space applications for anti-wasting drugs, as a safer alternative to steroids they will inevitably be hugely tempting for athletes too, not to mention the lazy as well. Although Goldberg is keen to point out that helping cheats and couch potatoes is not the focus of his work, he admits that it will undoubtedly happen sooner or later.

As the field of sleep research is still relatively new, scientists have yet to determine exactly why people sleep. However, they do know that humans must sleep and, in fact, people can survive longer without food than without sleep. And people are not alone in this need. All mammals, reptiles and birds sleep. Scientists have proposed the following theories on why humans require sleep:

Sleep may be a way of recharging the brain. The brain has a chance to shut down and repair neurons and to exercise important neuronal connections that might otherwise deteriorate due to lack of activity.

Sleep gives the brain an opportunity to reorganise data to help find a solution to problems, process newly-learned information and organise and archive memories.

Sleep lowers a person's metabolic rate and energy consumption.

The cardiovascular system also gets a break during sleep. Researchers have found that people with normal or high blood pressure experience a 20 to 30% reduction in blood pressure and 10 to 20% reduction in heart rate.

During sleep, the body has a chance to replace chemicals and repair muscles, other tissues and aging or dead cells.

In children and teenagers, growth hormones are released during deep sleep.

When a person falls asleep and wakes up is largely determined by his or her circadian rhythm, a day-night cycle of about 24 hours. Circadian rhythms greatly influence the timing, amount and quality of sleep.

For many small mammals such as rodents, sleep has other particular benefits, as it provides the only real opportunity for physical rest, and confines the animal to the thermal insulation of a nest. In these respects, sleep conserves much energy in such mammals, particularly as sleep can also develop into a torpor, whereby the metabolic rate drops significantly for a few hours during the sleep period. On the other hand, humans can usually rest and relax quite adequately during wakefulness, and there is only a modest further energy saving to be gained by sleeping. We do not enter torpor, and the fall in metabolic rate for a human adult sleeping compared to lying resting but awake is only about 5-10%.

A sizeable portion of the workforce is shift workers who work and sleep against their bodies' natural sleep-wake cycle. While a person's circadian rhythm cannot be ignored or reprogrammed, the cycle can be altered by the timing of things such as naps, exercise, bedtime, travel to a different time zone and exposure to light. The more stable and consistent the cycle is, the better the person sleeps. Disruption of circadian rhythms has even been found to cause mania in people with bipolar disorder.

The 'seven deadly sins' formulated by the medieval monks included Sloth. The Bible in Proverbs 6:9 includes the line: 'How long will you sleep, O sluggard? When will you arise out of your sleep?' But a more nuanced understanding of sloth sees it as a disinclination to labour or work. This isn't the same as the desire for healthy sleep. On the contrary, a person can't do work without rest periods and no one can operate at top performance without adequate sleep. The puritan work ethic can be adhered to and respect still paid to the sleep needs of healthy humans. It is wrong to see sleep as a shameful activity.

Usually, sleepers pass through five stages: 1, 2, 3, 4 and REM (rapid eye movement) sleep. These stages progress cyclically from 1 through REM then begin again. A complete sleep cycle takes an average of 90 to 110 minutes. The first sleep cycles each night have relatively short REM sleeps and long periods of deep sleep but later in the night, REM periods lengthen and deep sleep time decreases.

Stage 1 is light sleep where you drift in and out of sleep and can be awakened easily. In this stage, the eyes move slowly and muscle activity slows. During this stage, many people experience sudden muscle contractions preceded by a sensation of falling.

In stage 2, eye movement stops and brain waves become slower with only an occasional burst of rapid brain waves.

When a person enters stage 3, extremely slow brain waves called delta waves are interspersed with smaller, faster waves. In stage 4, the brain produces delta waves almost exclusively. Stages 3 and 4 are referred to as deep sleep, and it is very difficult to wake someone from them. In deep sleep, there is no eye movement or muscle activity. This is when some children experience bedwetting, sleepwalking or night terrors.

In the REM period, breathing becomes more rapid, irregular and shallow, eyes jerk rapidly and limb muscles are temporarily paralysed. Brain waves during this stage increase to levels experienced when a person is awake. Also, heart rate increases, blood pressure rises and the body loses some of the ability to regulate its temperature. This is the time when most dreams occur, and, if awoken during REM sleep, a person can remember their dreams. Most people experience three to five intervals of REM sleep each night.

Infants spend almost 50% of their time in REM sleep. Adults spend nearly half of sleep time in stage 2, about 20% in REM and the other 30% is divided between the other three stages. Older adults spend progressively less time in REM sleep.

As sleep research is still a relatively young field, scientists did not discover REM sleep until 1953, when new machines were developed to monitor brain activity. Before this discovery, it was believed that most brain activities ceased during sleep. Since then, scientists have also disproved the idea that deprivation of REM sleep can lead to insanity and have found that lack of REM sleep can alleviate clinical depression although they do not know why. Recent theories link REM sleep to learning and memory.