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Gene chips reveal changes in the hearts of gym rats
  
By Nancy Touchette

The exercise faithful who sweat up a storm on a daily basis know that working out is good for the heart. Healthy hearts perform better because their muscles contract more efficiently, and a new study begins to unravel the genetics of this process.


Rats who work out daily on a treadmill show improved heart function, apparently due to the increased activity of a gene encoding a special form of myosin.

Researchers at the University of Wisconsin-Madison have found that several dozen genes play a role in remodeling the heart—at least in laboratory rats on a training regimen. Gary M. Diffee and his colleagues used genomic tools to analyze the activity of genes in rats that go to the gym.

The researchers found significant changes in the activity of only 27 genes between the rats that exercised and their sedentary counterparts. They monitored the activity of nearly 9,000 rat genes using gene chips, or DNA microarrays.

"We were a bit surprised, at least initially, that there weren't a whole lot of substantial changes," says Diffee. "But when we thought about it more, we should have expected that. The heart is pretty well equipped to do most of what we ask it in endurance training." Exercise is not a severe stressor to the heart, he adds.

The researchers found that, among rats in training-up to one hour on the treadmill each day for nearly three months—ten genes in the ventricle of the heart showed increased activity and 17 genes showed decreased activity, compared to rats that did not exercise. The findings appear in the American Journal of Physiology - Heart and Circulatory Physiology.

Diffee found that with exercise training, the rats produce an embryonic form of a protein involved in muscle contraction. This protein, a component of a filament known as myosin, interacts with another filament made of the protein actin. The myosin slides along actin, causing a muscle fiber to contract.

Diffee and his colleagues also found changes in the ability of heart muscle to contract as a result of the training. Heart cells from the ventricles of trained rats contracted with a greater velocity and were more sensitive to calcium.

Why would a person need different forms of heart muscle proteins? If a person is exercising, Diffee notes, it might be helpful to produce muscle proteins that can pump blood at a higher rate. This requires more energy, however. Because a sedentary individual does not have the same circulatory needs, perhaps evolution has found a way to conserve energy by activating genes that produce less efficient myosin proteins, but require less energy.

As with many humans, the rats needed motivation to stick to their regimen, and this was not a trivial problem for the researchers. "They often don't feel like running," Diffee says. "We had to keep banging on the treadmill or shooting a stream of water at them. It required constant vigilance."

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Difee, G.M. et al. Microarray expression analysis of effects of exercise training reveals an increase in atrial myosin light chain 1 in rat ventricle. Am J Physiol Heart Circ Physiol Published online November 7, 2002.
 

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