New studies find exercise makes for better eye health, less chronic pain, stronger bones and can even help prevent some cancer. Image
When you put in hours at the gym, you expect to get fitter. It turns out, that assumption doesn't hold true for everyone. A new study suggests specific genes may determine, at least in part, how much we really benefit from exercise.
While "benefit from exercise" can mean plenty of things, from slimming down to boosting one's ability to complete a marathon, the researchers specifically looked at what is called VO2 max, or aerobic capacity. This is a measure of how much blood your heart pumps and how much oxygen your muscles consume when they constrict to, say, move your legs on a treadmill.
Bottom line, VO2 max represents your endurance. And this study, detailed today in the Journal of Applied Physiology, suggests a group of 29 genes could potentially categorize individuals into low, medium and high responders to exercise.
The researchers stress that exercise has benefits, regardless of whether or not a person can improve aerobic capacity. You can still lose weight, and other health factors such as cholesterol levels could benefit.
So-called low responders "may not see an improvement in their tolerance to exercise, or any improvement in their capacity to do the exercise, but their blood levels of cholesterol and lipids may improve quite substantially," said lead researcher Claude Bouchard, of the Pennington Biomedical Research Center in Baton Rouge, La.
In theory, the more you train, the better your body should get at using oxygen, and your VO2 max should increase. Indeed, elite athletes often have very high VO2 max's compared with average Joe.
However, about 20 years ago, some scientists started to question whether or not the link between training and fitness level was so clearcut. For instance, in the so-called Heritage family study, Bouchard and colleagues had about 500 relatively sedentary individuals train for 20 weeks between 1992 and 1997. Participants' ability to improve their fitness varied greatly lot, despite the fact that all participants rigorously adhered to the same exercise regime.
In that study, some people could increase their VO2 max up to 50 percent, while others saw no change. Since the study involved about 100 families, Bouchard's team could check to see if genetics was at play. Indeed, it was. Genes could account for about half of the difference they were seeing in people's ability to increase their VO2 max.
In other words, a good portion, but not all, of a person's capacity to get more fit was set by their heredity.
The question then became, what genes?
To find out, Bouchard and his colleagues, who came from 14 different institutions, used data from three separate exercise studies, including the Heritage.
They initially identified, using a novel approach, a set of 29 genes that seemed to predict a person's ability to improve their VO2 max. Then, they examined the individual DNA sequence of those genes, looking for differences in the genetic code. They found a total of 11 DNA differences, or markers, which appeared to be predictive of a person's ability to get fitter.
But these markers don't tell the whole story. Remember, heredity is only thought to account for 50 percent of a person's capacity to improve their fitness. Of this 50 percent, the newly identified genes can only explain about 23 percent of the variation in an individual's ability to be trained to improve VO2 max.
"With this we can identify, with a reasonable degree of precision, who is a low responder [to exercise], an average responder, or a high responder," Bouchard said. "We can begin to rank order people for their ability to be trained before they are trained."
In addition, in the Heritage study, the people who improved their fitness (VO2 max) the most weren't necessarily the ones who improved their blood pressure the most, or lowered their cholesterol. So these factors, which are thought to be indicators for heart disease risk, could be controlled by different genes, Bouchard said.
While Bouchard feels this study is a big step forward, more work is needed before it can have real-world applications, including finding more genes and then verifying the markers in other populations.
But down the road, the findings may have practical uses. For instance, if someone learns they are a "low responder" to exercise, they know they may need to be more aggressive with their training in order to see an increase in their endurance. It may also help out with job selection, if a job requires a high level of fitness.
While other scientists agree that the work is intriguing, and notable for its unique approach to find and verify genes, they feel more research is needed. "It's helpful to provide some insights, but it clearly leaves a lot of questions," said Paul Gordon, professor at the University of Michigan who specializes in preventive and rehabilitative exercise science.
For example, the actual genes identified in this study were different from those previously found to play a role in the exercise-VO2 max link. And scientists know very little about what these genes really do to cause physical improvements in the body.
"I think the question still remains as to how important these genes are in contributing to the improvements. What is the actual cause and effect that’s going on here?" Gordon said.
Furthermore, the study size was small, and Gordon would like to see if the results can be replicated on a larger scale, and among different demographics.
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