Wondering why other people seem to respond better than you to aerobic exercise and strength training? Why one workout/training programme works well for some and not others? Well the answer may be a molecular “switch” say scientists at Joslin Diabetes Center.
“We’ve identified an exercise-activated biological pathway that hasn’t been studied at all,” says Sarah Lessard, PhD, an Assistant Investigator in Joslin’s section of Clinical, Behavioral and Outcomes Research.
Studying lab animals and humans, Lessard and her colleagues discovered that a protein called c-Jun N-terminal kinase (JNK) helps to drive response to exercise. If JNK is activated during exercise it helps skeletal muscle growth. If it’s not activated, muscles improve their adaptation for endurance and aerobic capacity.
“It’s like a switch,” Lessard remarks. “If the switch is on, you’ll have muscle growth. If it’s turned off, you have endurance adaptation in the muscle.”
However the switch does not work the same in everyone, as the scientists found in some people endurance training can activate JNK in their leg muscles. This activation might prevent endurance adaptations, and it might explain why some people don’t respond as well to endurance exercise.
“If a hundred people do the exact same aerobic training programme, some will have huge improvements in aerobic capacity, and some will have little to no response,” Lessard says.
Lessard and her colleagues began their study with mice that had been genetically modified to knock out production of JNK in their muscles. These “JNK knockout” mice remain perfectly healthy and will run vigorously on wheels in their cages very much like normal mice.
But when compared to normal mice, the investigators found the mice with the JNK knocked out of them had a much higher increase in aerobic exercise capacity, along with higher levels of blood vessels and of a type of muscle fibre specialised to give endurance.
Next, the Joslin researchers ran an experiment that promotes muscle growth in animals. Normal mice doubled the mass of their affected muscles, but the JNK knockout mice didn’t increase their muscle mass nearly as much.
The Joslin investigators then collaborated with Vernon Coffey, associate professor of exercise and sports science at Bond University in Gold Coast, Queensland, Australia, on tests in healthy, human volunteers. Results from Coffey’s group indicated that similar biological mechanisms were at work.
The tests showed that JNK was highly activated in the muscles of humans lifting leg weights, a resistance exercise. In contrast, JNK generally was not activated in muscle when the volunteers performed cycling, an endurance exercise.
But a significant minority of test subjects did show some JNK activation in their leg muscles during endurance exercise. That activation might prevent endurance adaptations, and it might explain why some people don’t respond as well to endurance exercise.
“We’ve begun to figure out how muscle decides whether it will grow or adapt for endurance, which really hasn’t been known,” Lessard concluded.