A couch potato mouse model has been used by scientists at Sanford-Burnham Medical Research Institute to study muscle function.
Daniel Kelly and his colleagues found that these mice maintain normal activity and body weight but do not have the energy to exercise.
They report what happens when muscle tissue lacks PGC-1, a protein coactivator that muscles need to convert fuel into energy.
In obese individuals, PGC-1 levels drop, possibly further reducing a person's capacity to exercise - creating a vicious cycle. In this study, mice without muscle PGC-1 looked normal and walked around without difficulty, but could not run on a treadmill.
What happens is that the part of the cell that converts fuel into energy - can't function properly, so cells have to work harder to stay vigorous. This extra effort rapidly depletes carbohydrate fuel stores, leading to premature fatigue.
However, PGC-1-deficient couch potato mice were not obese and still respond normally to insulin - meaning they are not at risk for developing diabetes despite their sedentary lifestyles and mitochondrial problems.
This study dispels that notion, instead suggesting that perhaps malfunctioning mitochondria are a result of diabetes, rather than a cause.
"Lo and behold, even though these animals couldn't run, they showed no evidence of insulin resistance," Kelly said.
"We are now investigating what happens when we boost PGC-1 activity intermittently, as normally occurs when a person exercises."
The study appears in the December 1 issue of Cell Metabolism.