Charles Czeisler and his colleagues from Harvard Medical School, and
Brigham and Women’s Hospital, Boston, devised a routine to enable night
workers to adapt. They were building on an earlier discovery by Czeisler
that the ‘circadian pacemaker’ in humans can be reset by exposure to very
bright light (New ÐÓ°ÉÔ­´´, Science, 16 July 1989).

The routine involved exposing workers to bright light while they worked
at night, making sure that they stayed in complete darkness while resting
during the day. The researchers found that this helped people to adapt rapidly
to night work (New England Journal of Medicine, vol 1322, p 1253).

If people fail to adapt properly to night work, it can lead to several
problems. For instance, they tend to have more accidents at night due to
fatigue, and they perform tasks less effectively and are less alert. In
the day, insomnia can be a problem. According to some researchers, long-term
exposure to night work may even increase the risk of diseases, such as heart
disease.

Czeisler and his colleagues tested their routine on healthy young men
who were not regular night workers. Each night for a week, the men reported
to the laboratory for sedentary ‘work’. The rest of the time, they lived
normally in their homes.

The researchers carried out 10 separate studies. In five of the studies
which acted as controls, the men worked through the night in ordinary indoor
lighting, which corresponds to an intensity of about 150 lux. The men were
given no special instructions about how they should sleep during the day.

Czeisler and his colleagues dubbed the remaining five studies the ‘treatment’
group. The men in the group worked during the night in bright light, at
a level of 7000 to 12,000 lux. This is an intensity similar to that of early
morning light. After their work, the men were told to go home and remain
in darkness from 9 am to 5 pm.

Throughout the night, Czeisler’s team measured the body temperatures,
performance and alertness of their subjects. On the first and the sixth
days of the experiment, they made a full recording of these cycles, keeping
the men in the laboratory for 24 hours.

Researchers have long known that body temperature varies with the circadian
cycle. Sure enough, all the men in the treatment group experienced a drop
in body temperature at the start of the experiment. The drop occurred in
the early hours of the morning. The lowest temperature was around 5 am,
which was about two hours before the men usually woke.

By, by the sixth day, the men in the treatment group had experienced
a shift in their cycle of body termperature. The lowest temperature now
occurred about 10 hours later, at around 3 pm. However, in the control group,
the time of the lowest body temperature had moved forward by about one hour
only.

When Czeisler and his colleagues measured other biological functions,
such as the production of urine, they found that the men in the treatment
group had adapted their circadian rhythms to night work, whereas the men
in the control group had not.

After six nights, says Czeisler, those in the treatment group were significantly
more alert than those in the control group. They also performed tasks better,
he says. Czeisler believes that his treatment routine allows people to adapt
physically to night work within as little as four days.

According to Czeisler a nerve pathway in the brain is crucially important
in resetting the circadian pacemaker. The retinohypothalamic tract leads
from the retina – the part of the eye that receives light and visual images
– to an area in a part of the brain known as the hypothalamus, where the
pacemaker resides. It is through this tract, says Czeisler, that the circadian
pacemaker receives messages about cycles of light and dark in the outside
world.

According to Andrew Wade and his colleagues at the London Hospital Medical
College, this is the first study to link obesity and muscle fibres. The
findings could change our ideas about how useful it is to exercise in order
to lose weight.

Skeletal muscle makes up the body’s largest mass of tissue. Like all
human muscle it contains a mixture of fibres. These fibres differ in the
way that they generate energy in order to contract. ‘Slow’, or type 1, fibres
use fatty acids, the constituents of fat, as an important source of fuel.
There are stores of fat within the muscle fibres, so slow fibres are relatively
resistant to fatigue. Meanwhile, ‘fast’, or type 2, fibres readily use glucose
as a fuel, especially those fibres that are not adapted by regular exercise.

According to Wade, the relative proportions of the two different fibres
may vary widely from one individual to another. Slow fibres can compose
up to 96 per cent of the mass of the thigh muscle, the quadriceps, or as
little as 13 per cent. Wade says that the quadriceps is a good indicator
of the composition of the major skeletal muscles of an individual.

The researchers studied 11 healthy men, none of whom was particularly
athletic. They took samples of tissue from the quadriceps muscles and stained
them. The two types of fibre stained differently, allowing the researchers
to measure their relative proportions. Next, Wade and his colleagues compared
these proportions with estimates of the total body fat in each man. They
found that the leaner the man the greater the proportion of his slow fibres
in his quadriceps (The Lancet, vol 335, p 805).

It is possible to calculate the dominant type of fuel a muscle is using
by measuring how much oxygen it uses up and how much carbon dioxide it produces
during activity. Wade and his colleagues set out to do this. They used 50
healthy, but mostly sedentary, men, including the 11 from the first experiment.
They made the men do equal amounts of work.

Wade and his colleagues found that fatter men – and those with a higher
proportion of fat muscle fibres – burnt less fat than lean men, who had
a greater proportion of slow fibres. This, they say, suggests that the rate
at which the muscle burns fat is related both to how fat the individual
is and to the relative properties of slow and fast fibres in the muscle.

If, as the researchers have found, obese people have a greater proportion
of fast fibres in their muscles, this could explain why they may find it
difficult to start a programme of exercise, claims Wade. Not only do their
muscle fibres tire more easily, but they tend to burn less fat and more
glucose when they are working hard. He believes that these are important
factors in explaining why doctors are often unsuccessful when they try to
persuade people to take more exercise.

A person’s composition of muscle fibre cannot change, but every fibre
can be trained by exercise. After at least six weeks, Wade found that the
trained fast fibres behave much more like slow fibres.

Wade feels that if fat people understood the role of their muscle fibre
types, this could help to motivate them to persevere with exercise. He now
hopes to develop a way of determining a person’s relative proportions of
muscle fibres without taking a sample.

Penelope Ward of St Mary’s Hospital Medical School, London, and her
colleagues looked at the tissue of women undergoing routine cervical smear
tests. They reported their findings at the annual meeting of the British
Society for Colposcopy and Cervical Pathology, held in Sheffield.

The researchers suspected cervical cells might be damaged because previous
studies have found the constituents of cigarette smoke in the mucus which
coats them. Smoking could damage DNA in several ways. One way would be for
it to cause DNA ‘adducts’ – extra compounds – to form on the genetic material
of the cell. These adducts are products of the aromatic hydrocarbons in
smoke which bind to DNA. They are an early step in the development of cancer.

Previously, researchers have detected adducts in the DNA of cells of
the lungs and placental tissue of smokers. Those who smoked the most showed
the most damage.

Ward and her colleagues studied 22 women. They measured the quantities
of DNA adducts in tissue obtained from cervical smears. Thirteen of the
women were currently smoking; nine had never smoked.

The nonsmokers had no adducts or adducts at low levels only. Of the
smokers, two-thirds had levels of adducts in the same range as the nonsmokers,
but three of the smokers had very high levels of adducts indeed. Ward and
her colleagues now want to know whether these smokers are a subgroup of
smokers specially at risk of developing cancer, or precancerous changes,
to the cervix. To test this, they now hope to look at adduct levels in patients
with established invasive cervical cancer. Stephanie Taylor