It means that people with more myostatin have less muscle mass, and people with less myostatin have more muscle mass.
Study leader Dr Joshua Butcher, a postdoctoral fellow at the Vascular Biology Center at Augusta University in Georgia, said: "Given that exercise is one of the most effective interventions for obesity, this creates a cycle by which a person becomes trapped in obesity."
Obesity is linked with several factors that increase the risk of heart disease and diabetes, including high blood pressure, high cholesterol, insulin resistance and kidney damage.
The researchers bred four groups of mice: lean and obese mice with uninhibited myostatin production and lean and obese mice that were unable to produce myostatin.
As expected, mice that were unable to produce myostatin developed markedly higher muscle mass, though the obese mice remained obese even with more muscle.
The obese mice that were unable to produce myostatin showed markers of heart and metabolic health that were on a par with their lean counterparts and dramatically better than obese mice with uninhibited myostatin production.
Dr Butcher said: "In our muscular obese mouse, despite full presentation of obesity, it appears that several of these key pathologies are prevented.
"While much more research is needed, at this point myostatin appears to be a very promising pathway for protection against obesity-derived cardiometabolic dysfunction."
He added: "Ultimately, the goal of our research would be to create a pill that mimics the effect of exercise and protects against obesity.
"A pill that inhibits myostatin could also have applications for muscle wasting diseases, such as cancer, muscle dystrophy and AIDS."
He was due to present the findings at the American Physiological Society's annual meeting in Chicago.
But scientists also point out that it could be a major development in treating obese people, since studies suggest their bodies overproduce myostatin, making it harder to see results from exercise.
The researchers zeroed in on myostatin because it is known as a powerful inhibitor of skeletal muscle growth.
It means that people with more myostatin have less muscle mass, and people with less myostatin have more muscle mass.
Study leader Dr Joshua Butcher, a postdoctoral fellow at the Vascular Biology Center at Augusta University in Georgia, said: "Given that exercise is one of the most effective interventions for obesity, this creates a cycle by which a person becomes trapped in obesity."
Obesity is linked with several factors that increase the risk of heart disease and diabetes, including high blood pressure, high cholesterol, insulin resistance and kidney damage.
The researchers bred four groups of mice: lean and obese mice with uninhibited myostatin production and lean and obese mice that were unable to produce myostatin.
As expected, mice that were unable to produce myostatin developed markedly higher muscle mass, though the obese mice remained obese even with more muscle.
The obese mice that were unable to produce myostatin showed markers of heart and metabolic health that were on a par with their lean counterparts and dramatically better than obese mice with uninhibited myostatin production.
Dr Butcher said: "In our muscular obese mouse, despite full presentation of obesity, it appears that several of these key pathologies are prevented.
"While much more research is needed, at this point myostatin appears to be a very promising pathway for protection against obesity-derived cardiometabolic dysfunction."
He added: "Ultimately, the goal of our research would be to create a pill that mimics the effect of exercise and protects against obesity.
"A pill that inhibits myostatin could also have applications for muscle wasting diseases, such as cancer, muscle dystrophy and AIDS."
He was due to present the findings at the American Physiological Society's annual meeting in Chicago.
