News ID: 219315
Published: 0931 GMT August 04, 2018

Molecular 'switch' controling how much muscle we build

Molecular 'switch' controling how much muscle we build

To the frustration of many gym-goers, some people can build and maintain muscles with little to no effort, while others have to work twice as hard for half the results.

What's responsible for this difference in response to exercise? New research sheds light, according to

Exercise in general is excellent for health, and muscle-strengthening activities in particular have specific health benefits.

These range from a lower risk of premature mortality to a stronger, healthier brain in later life.

But some of us build muscles much more easily than others. A new study, which now appears in the journal Nature Communications, offers a molecular explanation for why that is.

The new research also explains why some people seem to respond better to endurance training and aerobic exercise rather than muscle training.

Sarah Lessard, PhD — an assistant investigator in the clinical, behavioral and outcomes research section of the Joslin Diabetes Center in Boston, MA — is the first author of the paper.

The molecule in question is a protein called c-Jun N-terminal kinase (JNK).

Speaking of it, Lessard said, "It's like a switch [...] If the switch is on, you'll have muscle growth. If it's turned off, you have endurance adaptation in the muscle."

she added, "We've identified an exercise-activated biological pathway that hasn't been studied at all." 


How JNK influences muscle growth


The new study builds on previous work that the same scientists conducted. In their previous study, Lessard and colleagues examined the genetic makeup of rodents they had bred to respond very well or very poorly to endurance exercise.

It was then that the researchers first discovered that the JNK molecular pathway was responsible for how well a mouse would perform on the treadmill.

In the new study, the researchers wanted to know more about the reasons why JNK would have such a vital role.

So, Lessard and team knocked out the JNK gene in a group of mice and compared their behavior with that of normal mice.

The knockout rodents remained healthy and continued to run on the treadmill for long periods of time.

Next, the researchers trained both groups of rodents to run. This was when the scientists remarked that the aerobic capacity of the JNK-free mice had increased drastically, along with their blood vessels and a muscle fiber that builds endurance.

By contrast, in a muscle growth experiment, JNK-free rodents failed to increase their muscle mass, whereas regular mice doubled theirs.


Muscle-building protein linked with diabetes


The new research also included tests in humans. Lessard and colleagues asked healthy volunteers to engage in either weight-lifting exercise or cycling, a type of endurance workout.

The tests found that JNK was highly active in the former kind of exercise but not active in the latter.

Because studies also found JNK to be implicated in metabolic inflammation, the researchers hope that inhibiting this pathway will prevent metabolic conditions such as type 2 diabetes.

Also, the findings may help those who want to build muscle but cannot because of various diseases.


Security Key:
Captcha refresh
Page Generated in 0/0417 sec