Cyclin D1 as a Potential Basis for an Exercise Mimetic
Researchers continue to delve into the mechanisms by which exercise produces benefits in older individuals, with an eye to producing exercise mimetic drugs. The study here is an example of the type, comparing some of the biochemistry of exercise in young, old, exercising, and sedentary mice. This part of the field is likely to evolve in much the same way as the development of calorie restriction mimetics over the past twenty years - slowly, in other words. Cellular metabolism is very complex, and picking out target mechanisms has a fair rate of failure.
Researchers gave mice that were about 20 months old, the equivalent of being 60-70 years old in humans, and mice that were 3 to 4 months old, the equivalent of 20- to 30-year-old humans, access to an exercise wheel and allowed them to run at will. Young mice averaged about 10 kilometers each night, and the older mice covered about 5 kilometers. Two other groups of young and old mice were given wheels that didn't rotate to serve as controls.
Subsequent analysis showed that the muscle stem cells of the exercising animals remained quiescent, and that the animals did not develop significant numbers of new muscle fibers in response to the exercise. After three weeks of nightly aerobics for the active groups, the researchers compared the ability of the animals to repair muscle damage. They found that, as expected, the aged, sedentary mice were significantly less able to repair muscle damage than younger sedentary mice. However, the older animals that had exercised regularly were significantly better at repairing muscle damage than were their counterparts that did not exercise. This exercise benefit was not observed in the younger animals.
The researchers also showed that injecting blood from an old mouse that had exercised into an old mouse that hadn't conferred a similar benefit in stem cell function, suggesting that exercise simulates the production of some factors that then circulate in the blood and enhance the function of older stem cells. Further studies indicated that the exercise-induced rejuvenation observed by the researchers could be mimicked by increasing the expression of a signaling molecule called cyclin D1, which is involved in rousing resting muscle stem cells in response to damage. The discovery suggests that it may one day be possible to artificially activate this pathway to keep aging muscle stem cells functioning at their youthful best.
While it is not likely that this compound will replace be exercise it might be useful as exercise enhancer. Say instead of 1 h workout 40 be minutes might give the same benefit with an enhancer. .. or the effects might not coming that well...