Washington, July 17 : Are you a couch potato who hates getting up and working out? Well, as it turns out you may just be able to blame your genes for your lazy disposition.
While working out is known to be the key to manage good health, two new studies suggest that the inclination to engage in physical activity may be strongly affected by genetics.
While not much research has been done into the effects of genetics on human activity, recent studies on mice have indicated strong genetic influences.
In one of the recent studies a team led by University of North Carolina at Charlotte kinesiologist J. Timothy Lightfoot identified six locations on the mouse chromosome where differences had a strong relationship to activity, indicating at least six genes that individually can affect activity.
A second genetic study by the same team found seventeen other genetic locations that were also having an effect on activity levels by interacting with each other, a genetic effect known as epistasis.
Taken together, the located genes account for approximately 84pct of the behavioural differences between mice that exhibit low activity levels and mice that show high activity traits.
"Can you be born a couch potato? In exercise physiology, we didn't used to think so, but now I would say most definitely you can," said Lightfoot.
Lightfoot worked with strains of mice that had markedly different behaviours when given an exercise wheel. A "high-active" strain scored notably higher than other strains in speed, duration and distance achieved in running than other strains, including one that was labeled as "aggressively sedentary" because of its consistent avoidance of activity.
Initially, Lightfoot suspected that the difference was due to genetic factors affecting the way energy is used by muscle tissue because early genetic studies of the strains indicated that variation was present in genes known to affect metabolism. However, studies on muscle tissue in the different mice failed to show a genetic effect that could cause a difference in muscle performance.
"We have done some gene chips on muscle tissue and we don't see any differential expression between high-active and low-active animals in peripheral (muscle) tissue. So the suggestion that by over-expressing a glucose transporter we can increase activity doesn't seem to be the explanatory factor," said Lightfoot.
Subsequent studies indicated that genetic differences are having a profound affect on mouse activity levels by causing significant differences in their brains.
"More and more what we are seeing is differences in brain chemistry. We are really convinced now that the difference is in the brain. There is a drive to be more active," said Lightfoot.
The current studies interbred active and inactive strains of mice to re-sort the genes. The researchers tested the second generation (f2) of offspring for activity using three measurements -- speed, endurance and distance - and found a range of significant differences among the new hybrid mice in their overall activity levels. The team then performed genetic tests on the mice and found significant correlations between differences in their genomes and the behavioral variations.
While differences in activity could not be exclusively connected to genetics, a surprisingly large amount of the activity difference in the hybrids - about half - had a strong relationship to the specific genetic variations identified.
"We don't know yet what the genes involved in activity are doing, but there is some strong suggestion that many of them may be involved in regulating dopamine. In one sense it is very similar to a model for genetic influences on ADD," noted Lightfoot.