Exploring Why Some People Get Fitter Than Others
By Gretchen Reynolds
Anyone in a running
group or gym class has likely noticed that some of the participants
annoyingly become much fitter than others. But exactly why some people’s
bodies respond well to working out and others do not puzzles
scientists.
Studies indicate,
unsurprisingly, that genetics must be involved, since a particularly
high or low response to exercise tends to run in families. But less has
been known about which genes might be involved, and how those genes
actually increase or blunt the body’s response.
Now a new study in
rats adds to a growing body of data about how and why bodies respond so
differently to exercise. In the study, rats with a particular set of
genes responded robustly to exercise, becoming much more fit after a few
weeks of running, while rats born with other genes gained little
cardiovascular benefit from the same exercise program, apparently
because their heart muscles didn’t react as expected.
The results raise
questions about whether people who remain stubbornly unfit, no matter
how diligently they work out, might want to rethink their exercise
routines.
Anyone who closely
examines the results of exercise-related experiments will notice that
some participants get more physical bang from exercise than others. The
range of response can be startlingly broad.
In a telling study published in March,
for instance, 95 older, overweight men and women began five months of
endurance or weight training. By the end of that time, the volunteers
were, on average, 8 percent stronger or more aerobically fit (depending
on which program they had followed). But 13 percent of those in the
endurance group had lost aerobic capacity, and 30 percent of those in
the strength-training group were weaker.
For the new rodent study,
which was published this month in The Journal of the American College
of Cardiology, scientists from the University of Michigan in Ann Arbor
and the Norwegian University of Science and Technology in Trondheim
created two strains of rats that would or would not respond well to
working out.
To do so, they first
had rats run for several weeks and noted how much distance the animals
added before tiring during that time, meaning how well they were
adapting to the workouts.
The males that added
the most mileage were bred with the females who responded likewise, and
the animals that added the fewest miles to their runs were also mated to
one another.
After seven generations, the scientists had rats that should have been high or low responders to exercise.
And the first part of
the new experiment proved that supposition to be true. The two types of
rats were set on teensy treadmills with workouts that were identical in
speed and intensity. The animals completed the same training program for
two months.
By the end, the rats
bred to respond well to running had increased the distance that they
could run before tiring by about 40 percent.
The other rats were much more resistant to training, generally losing about 2 percent of their endurance during the training.
Next the scientists
examined the animals’ hearts, since differences in cardiovascular
responses to exercise could be expected to originate there. Normally,
the left ventricle of the heart in animals and people becomes larger and
able to contract more forcefully after a period of endurance training.
So it was among the
high-responding rats. Cells from their left ventricles showed structural
changes associated with growth and strength. They were developing
athletes’ hearts.
Not so the other rats.
Cells from their left ventricles looked like those from animals that
hadn’t run. There were almost no physiological adaptations.
This cellular
intractability likely explains why the animals lost fitness while
training, says Ulrik Wisloff, a professor at the Norwegian University of
Science and Technology who led the new study.
If hearts don’t adapt to
the demands of exercise, then workouts will sap bodies, not strengthen
them.
But perhaps the most
fascinating aspect of the new study involved the scientists’
determination of the gene activity driving these adaptations. When they
carefully assessed gene expression in the animals’ heart cells, they
found more than 360 genes that were operating differently in the two
groups of animals. Many of these genes are known to affect cell growth.
In effect, these genes
direct processes that should increase the size and strength of the
heart. And they were not working as effectively in the animals bred to
be resistant to exercise.
Humans have these same
genes in our heart cells, Dr. Wisloff said, although it is impossible
at this point to know if our genes respond in precisely the same way
during exercise as the genes of the rats did, Dr. Wisloff said.
He also pointed out
that the interplay of genes and exercise is extremely complex, and
scientists are only in the earliest stages of understanding the effects
of heredity, environment, nutrition and even psychology in affecting
different people’s responses to exercise.
But the potential
lesson of the new study would seem to be, he said, that we should
closely monitor our body’s response to exercise. If after months of
training, someone is not able to run any farther than he or she could
before, maybe it is time to change the intensity or frequency of the
workouts or try something else, like weight training. The genes that
control the body’s responses to that activity are likely to be very
different than those involved in responses to aerobic exercise, Dr.
Wisloff said.