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How Exercise Grows a Healthy Heart

January 5, 2011

(Ivanhoe Newswire) — It’s common knowledge that exercise offers metabolic and cardiovascular benefits; however, scientists surprisingly know little about how physical activity actually influences the heart itself. Thanks a new study, scientists now know a little more.

Mice in the study that exercised turned on a genetic program that leads the heart to grow as heart muscle cells divide. In due course, the shift in activity is driven, in part, by a solitary transcription factor (a gene that controls other genes). That gene, commonly referred to as C/EBPb, was known to play imperative roles in various other parts of the body, although this is the foremost evidence for its influence in the heart.

“We’ve identified a pathway involved in beneficial cardiac hypertrophy — the good kind of heart growth,” Bruce Spiegelman of Harvard Medical School, was quoted as saying.

These discoveries might offer clinical implications, predominantly for those with heart failure or other conditions that make exercise demanding to impossible.

“This is yet another reason to keep on exercising,” Anthony Rosenzweig of Harvard Medical School, was quoted as saying. “In the longer-term, by understanding the pathways that benefit the heart with exercise, we may be able to exploit those for patients who aren’t able to exercise. If there were a way to modulate the same pathway in a beneficial way, it would open up new avenues for treatment.”

There may be additional ways to optimize training regimens so that they tap into this natural mechanism more proficiently, Spiegelman added. The heart muscle adapts to increased pressure and volume by increasing in size, according to the researchers. This is true in the case of exercise as it is in pathological conditions including high blood pressure. In disease states as opposed to exercise, those changes to the heart can eventually lead to heart failure and arrhythmias.

Researchers discovered changes in 175 transcription factors in exercised mice and 96 in mice whose aortas were constricted. Notably, the changes illustrated slight overlap between the two animal models. For instance, the researchers said, 13 percent of the genes with differential expression subsequent to exercise have known or suggested roles in cell production in comparison to less than 1 percent of those that changed with the surgery.

The researchers then zeroed in on one transcription factor, C/EBPb, which goes down roughly two-fold with exercise and a second that rises in turn. Studies in animals and cell culture additionally illustrated that the decline in C/EBPb leads to transformations that appear to be constant with those that follow endurance exercise, including an increase in both heart muscle size and proliferation. Those mice with lower C/EBPb levels as well were resilient to heart failure.

Researchers add that these findings are principal for the fact that there is exceptionally little prior evidence demonstrating that the increase in heart size with exercise has direct benefits. The innovative evidence also gives essential biological insights into the heart’s capability for regeneration of muscle.

It will be key in future studies to investigate all of the players in the pathway and to offer even more authoritative evidence that exercise leads to an increased rate of cell proliferation in heart muscle, according to Rosenzweig.

SOURCE: Cell, December 2010