The muscle energy improvement wasn’t because people lost weight or got more active — it seemed to be linked directly to IGF-I levels instead.

Before starting the study, both the drug group and the placebo group had the same muscle energy recovery ability, so any later differences weren’t due to starting out differently.

We know muscle energy recovery got better, but we don’t know if it’s because there are more mitochondria, bigger ones, or just ones that work better.

The drug didn’t make muscles stronger or change how much energy they used during exercise — only how fast they recovered afterward, which points to mitochondria being the target.

The muscle energy recovery speed (ViPCr) responded more clearly to IGF-I than another measure (τPCr), meaning ViPCr might be a better way to track how well muscles are making energy.

Because so few people finished the study and the muscle energy didn’t improve much more in the drug group than the placebo group, we can’t say for sure the drug caused the improvement.